Author: "B, Van der Auwera" - Searchworks@Jio Institute Digital Library Search Results

66 results on '"B, Van der Auwera"'

1. IDF2022-0660 Non-HLA polymorphisms diversely impact progression of preclinical islet autoimmunity in distinct subgroups and stages

Author: J. Vandewalle, B. Van der Auwera, A. Desouter, B. Keymeulen, F. Gorus, and M. Van de Casteele
Subjects: Endocrinology, Endocrinology, Diabetes and Metabolism, Internal Medicine, General Medicine
Published: 2023
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2. Frequency of the phenylalanine deletion (ΔF508) in the CF gene of Belgian cystic fibrosis patients

Author: L Vits, Jan Wauters, K L Stuer, P. J. Willems, B. Van der Auwera, L van Schil, Paul Coucke, Jan Hendrickx, Jan E. Dumon, and A Van Elsen
Subjects: congenital, hereditary, and neonatal diseases and abnormalities, Cystic Fibrosis, Phenylalanine, Population, Biology, Polymerase Chain Reaction, Cystic fibrosis, law.invention, Belgium, Gene Frequency, law, Genetics, medicine, Humans, ΔF508, education, Gene, Allele frequency, Genetics (clinical), Polymerase chain reaction, education.field_of_study, Haplotype, medicine.disease, respiratory tract diseases, Haplotypes, Chromosome Deletion, Restriction fragment length polymorphism, Oligonucleotide Probes, Polymorphism, Restriction Fragment Length
Abstract: Cloning and sequencing of the CF gene has identified a three-base-pair deletion (delta F508) responsible for CF in the majority of CF patients (Kerem et al. 1989). We have used the polymerase chain reaction with oligonucleotide primers bridging the delta F508 deletion to analyze the presence or absence of this mutation in the Belgian CF population. The delta F508 mutation was present in 80% (57 on 71) of CF chromosomes from 36 unrelated Belgian CF families from the region of Antwerp. This mutation was associated with haplotype B for the KM.19-XV-2c RFLPs as 93% (53 on 57) of the CF chromosomes with the delta F508 mutation carried haplotype B.
Published: 2008
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3. Neither an intronic CA repeat within the CD48 gene nor the HERV-K18 polymorphisms are associated with type 1 diabetes

Author: S Ghebru, J. Herwig, B. Van der Auwera, J. Van Autreve, Folefac Aminkeng, Erhard Seifried, Klaus Badenhoop, Christian Seidl, Elizabeth Ramos-Lopez, Medical Biochemistry, and Pathologic Biochemistry and Physiology
Subjects: Male, Linkage disequilibrium, Genotype, type 1 diabetes, viruses, Immunology, Endogenous retrovirus, Disease, CD48 Antigen, Biology, Biochemistry, Linkage Disequilibrium, Antigens, CD, Genetics, medicine, Humans, Immunology and Allergy, Genetic Predisposition to Disease, Child, Dinucleotide Repeats, CD48, Type 1 diabetes, Polymorphism, Genetic, Superantigens, Endogenous Retroviruses, Haplotype, Case-control study, Membrane Proteins, General Medicine, medicine.disease, Introns, Diabetes Mellitus, Type 1, Case-Control Studies, Child, Preschool, embryonic structures, Female, HERV-K18, TCF7L2, Software
Abstract: Type 1 diabetes is an autoimmune heterogeneous disease that is determined by environmental and genetic factors. A possible retroviral etiology has been inferred from the observation that human endogenous retrovirus (HERV)-K18 encoding a superantigen (SAg) has a polymorphism associated with this disease. Type 1 diabetes families from Germany and Belgium were genotyped for the novel HERV-8914 (303 families) and for the known HERV-8594 (284 families) polymorphisms within the SAg-coding region on the HERV-K18. Case-control analysis was performed for the HERV-8914 polymorphism (506 patients) and for the HERV-8594 polymorphism (370 patients) and compared with 350 German controls. Haplotypes were constructed. Additionally, a microsatellite within the CD48 gene was analyzed in German type 1 diabetes families (n=125) as well as in patients (n=375) and in healthy controls (n=350). No association was found for HERV-K18 polymorphisms or the CA repeat within the CD48 gene with type 1 diabetes mellitus either in families or by comparing patients and controls. In conclusion, we cannot confirm a role of HERV-K18 polymorphisms -HERV-8914 and HERV-8594- or of the CD48 CA repeat for type 1 diabetes susceptibility.
Published: 2006
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4. Seasonality in clinical onset of Type 1 diabetes in Belgian patients above the age of 10 is restricted to HLA-DQ2/DQ8-negative males, which explains the male to female excess in incidence

Author: I Weets, M. Coeckelberghs, Z Laron, Eric Weber, L Kaufman, L Crenier, B. Van der Auwera, Daniel Pipeleers, R. Rooman, C De Block, Kristina Casteels, and F. K. Gorus
Subjects: Adult, Genetic Markers, Male, medicine.medical_specialty, Adolescent, Genotype, Endocrinology, Diabetes and Metabolism, Physiology, Disease, Biology, Belgium, HLA-DQ Antigens, HLA-DQ, Epidemiology, Internal Medicine, medicine, Humans, Prospective Studies, Registries, Age of Onset, Child, Prospective cohort study, Autoantibodies, Sex Characteristics, Type 1 diabetes, Incidence (epidemiology), medicine.disease, Diabetes Mellitus, Type 1, Immunology, Female, Seasons, Age of onset, Sex characteristics
Abstract: Type 1 diabetes arises from an interplay between environmental and genetic factors. The reported seasonality at diagnosis supports the hypothesis that currently unknown external triggers play a role in the onset of the disease. We investigated whether a seasonal pattern is observed at diagnosis in Belgian Type 1 diabetic patients, and if so whether seasonality varies according to age, sex and genetic risk, all known to affect the incidence of Type 1 diabetes.The seasonal pattern at clinical diagnosis was assessed in 2176 islet antibody-positive diabetic patients aged 0 to 39 years diagnosed between 1989 and 2000. Additional stratification was performed for age, sex and HLA-DQ genotype.Overall, a significant seasonal pattern at clinical diagnosis of diabetes was observed (p0.001). More subjects were diagnosed in the period of November to February (n=829) than during the period of June to September (n=619) characterised by higher averages of maximal daily temperature and daily hours of sunshine. However, the seasonal pattern was restricted to patients diagnosed above the age of 10 (0-9 years: p=0.398; 10-19 years: p0.001; 20-29 years: p=0.003; 30-39 years: p=0.015). Since older age at diagnosis is associated with a male to female excess and a lower prevalence of the genetic accelerator HLA-DQ2/DQ8, we further stratified the patients aged 10 to 39 years (n=1675) according to HLA-DQ genotype and sex, and we found that the seasonal pattern was largely restricted to male subjects lacking DQ2/DQ8 (n=748; p0.00 vs all others: n=927; p=0.031).In a subgroup of male patients diagnosed over the age of 10, the later stages of the subclinical disease process may be more driven by sex- and season-dependent external factors than in younger, female and genetically more susceptible subjects. These factors may explain the male to female excess in diabetes diagnosed in early adulthood.
Published: 2004
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5. Non-transmitted maternal HLA DQ2 or DQ8 alleles and risk of Type I diabetes in offspring: the importance of foetal or post partum exposure to diabetogenic molecules

Author: M. A. Pani, J. Van Autreve, B. Van der Auwera, Klaus Badenhoop, and F. K. Gorus
Subjects: Male, musculoskeletal diseases, Offspring, Endocrinology, Diabetes and Metabolism, Mothers, Human leukocyte antigen, Nuclear Family, Fathers, Genomic Imprinting, HLA-DQ Antigens, Diabetes mellitus, Internal Medicine, Humans, Medicine, Allele, Risk factor, skin and connective tissue diseases, Alleles, Sex Characteristics, business.industry, Haplotype, HLA-DQ2, nutritional and metabolic diseases, medicine.disease, Pedigree, Diabetes Mellitus, Type 1, In utero, Immunology, Female, business
Abstract: Type I (insulin-dependent) diabetes mellitus results from an immune-mediated destruction of pancreatic beta cells for which HLA haplotypes DR3-DQ2 and DR4-DQ8 represent the strongest genetic risk markers. Mothers of patients with rheumatoid arthritis carry more frequently the HLA DR4-DQ8 haplotype as non-transmitted haplotype than mothers of healthy control subjects. As maternal cells have been shown to persist in their offspring up to 30 years after birth, we investigated whether the association of HLA DR3-DQ2 and DR4-DQ8 with Type I diabetes is purely a genetic effect acting through inheritance or whether it can also act as an environmental factor, for example through foetal exposure in utero to maternal circulating cells.We analysed the non-transmitted parental HLA DQ alleles of 464 families (1367 subjects) with a Type I diabetic offspring. HLA DQ alleles were assessed using sequence-specific primers and allele-specific oligonucleotides hybridisation. A chi-square test was done to compare allele and transmission frequencies in the respective subsets of families.The non-transmitted HLA DR3-DQ2 and DR4-DQ8 were more frequent in mothers than in fathers of all non- DQ2/DQ8 heterozygous diabetic offspring ( p=0.0001) as well as in offspring not carrying any HLA high-risk allele ( p=0.0243). In patients with either risk allele alone, more maternal than paternal non-transmitted risk alleles complemented the constellation to DQ2/DQ8 ( p0.0099).HLA high risk alleles were more frequent among maternal non-inherited (but possibly exposed) alleles than among paternal non-inherited alleles. These results indicate that HLA DR-DQ is an environmental risk factor for Type I diabetes.
Published: 2002
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6. A retroviral long terminal repeat adjacent to the HLA DQB1 gene (DQ-LTR13) modifies Type I diabetes susceptibility on high risk DQ haplotypes

Author: K. H. Usadel, Ralf R. Tönjes, M. A. Pani, F. Gorus, C. Seidl, Klaus Badenhoop, B. van der Auwera, and K. Bieda
Subjects: Male, Endocrinology, Diabetes and Metabolism, HLA-DQB1 Gene, Human leukocyte antigen, Biology, Polymerase Chain Reaction, White People, Nuclear Family, Genomic Imprinting, Belgium, Germany, HLA-DQ Antigens, Diabetes mellitus, Internal Medicine, medicine, HLA-DQ beta-Chains, Humans, Genetic Predisposition to Disease, Gene, DNA Primers, Genetics, Base Sequence, Haplotype, Terminal Repeat Sequences, Chromosome, medicine.disease, Long terminal repeat, Diabetes Mellitus, Type 1, Haplotypes, Female, TCF7L2
Abstract: HLA-DQ genes, located in the human leukocyte antigen region on chromosome 6 p, are the main inherited factors predisposing to Type I (insulin-dependent) diabetes mellitus. Endogenous retroviral long-terminal repeats are integrated at several sites within this region, one of which is known to enhance susceptibility for Type I diabetes. We examined another LTR within the HLA-region as an additional genetic risk marker.We investigated the segregation of one long-terminal repeat (DQ-LTR13), located 1.3 kb upstream of HLA DQB1 with different HLA-DQ haplotypes, and its transmission to patients. A total of 284 Caucasian families (203 German and 81 Belgian) with at least one diabetic offspring were genotyped for DQA1, DQB1 and DQ-LTR13.DQ8/LTR13(+) was preferentially transmitted (139 transmitted vs 28 not transmitted; P(TDT) = 1.67 x 10(-14)) whereas no deviation from expected transmission frequencies was observed for DQ8/LTR13(-) (20 transmitted vs 17 not transmitted; P(TDT) = 1.00). DQ8/LTR13(+) alleles conferred a significantly higher risk for Type I diabetes than DQ8/LTR13(-) alleles (p chi(2) = 2.58 x 10(-14)). This difference remained significant even after DRB1 subtyping (p chi(2) = 0.02). Also, there was a significant difference when comparing the transmission of DQ2/LTR13(+) and DQ2/LTR13(-) alleles (p chi(2) = 0.01), the latter conferring an increased risk. The transmission of DQ-LTR13(+) haplotypes did not show any differences regarding paternal, maternal or gender-related stratification. However, DQ8/LTR13(-) was significantly more often transmitted from mothers (p chi(2) = 0.01) and to female patients (p chi(2) = 0.04).We conclude that DQ-LTR13 marks additional genetic risk for Type I diabetes on predisposing DRB1(*)0401- DQ8 and DQ2 haplotypes and will help to further define susceptibility in this gene region.
Published: 2002
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7. HLA-DRB1*04 and susceptibility to type 1 diabetes mellitus in a German/Belgian family and German case-control study

Author: T. Siegmund, Klaus Badenhoop, Horst Donner, B. Van der Auwera, C. Seidl, I. Weets, K. H. Usadel, J. Herwig, and J. Braun
Subjects: musculoskeletal diseases, Proband, medicine.medical_specialty, endocrine system diseases, Immunology, Population, Biochemistry, immune system diseases, Internal medicine, Genetics, medicine, Immunology and Allergy, Allele, skin and connective tissue diseases, education, HLA-DRB1, education.field_of_study, Type 1 diabetes, HLA-DQB1, business.industry, Haplotype, Case-control study, nutritional and metabolic diseases, General Medicine, medicine.disease, business
Abstract: HLA-DR4 is a primary disease association marker in type 1 diabetes mellitus (IDDM). We therefore analyzed the transmission of 228 DR4+ haplotypes in 183 families with an IDDM proband (95 from Germany and 88 from Belgium). In a separate case-control data set, we investigated the HLA-DRB1*04 and DQ allele distribution in 245 IDDM patients and 177 controls from Germany, all DR4 positive. HLA-DRB1 *0401 and *0402 linked to DQB1 *0302 were significantly more often transmitted to patients in the studied families (81% and 89%) in contrast to DRB1 *0401-DQB1 *0301 (33%). The case-control study of HLA-DQB1 *0302+ individuals revealed -DRB1 *0405 to be more frequent in patients with IDDM and HLA-DRB1 *0403 and -DRB1 *0404 to be less frequent. HLA-DQA1 *0102-DQB1 *0602 and -DQA1 *0501-DQB1 *0301 in trans complementation with DRB1 *0401-DQB1 *0302 were also significantly less frequent in IDDM patients (P
Published: 2000
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8. The Presence or Absence of a Retroviral Long Terminal Repeat Influences the Genetic Risk for Type 1 Diabetes Conferred by Human Leukocyte Antigen DQ Haplotypes

Author: I Weets, Reinhard Kurth, K. H. Usadel, B. van der Auwera, J. Herwig, Ralf R. Tönjes, Horst Donner, J. Braun, T. Siegmund, and Klaus Badenhoop
Subjects: musculoskeletal diseases, Genetics, HLA-DQB1, endocrine system diseases, Endocrinology, Diabetes and Metabolism, Biochemistry (medical), Clinical Biochemistry, Haplotype, nutritional and metabolic diseases, Human leukocyte antigen, Biology, Biochemistry, Long terminal repeat, Endocrinology, immune system diseases, Genetic marker, HLA-DQ, Genetic predisposition, skin and connective tissue diseases, HLA-DRB1
Abstract: Major genetic susceptibility to type 1 diabetes mellitus maps to the human leukocyte antigen (HLA) region on chromosome 6p. During evolution, endogenous retroviral long terminal repeats (LTR) have been integrated at several sites within this region. We analyzed the presence of a solitary HERV-K LTR in the HLA DQ region (DQ-LTR3) and its linkage to DRB1, DQA1, and DQB1 haplotypes derived from 246 German and Belgian families with a patient suffering from type 1 diabetes mellitus. Segregation analysis of 984 HLA DQA1/B1 haplotypes showed that DQ-LTR3 is linked to distinct DQA1 and DQB1 haplotypes but is absent in others. The presence of DQ-LTR3 on HLA DQB1*0302 haplotypes was preferentially transmitted to patients from heterozygous parents (82%; P < 10(-6)), in contrast to only 2 of 7 DQB1*0302 haplotypes without DQ-LTR3. Also, the extended HLA DRB1*0401, DQB1*0302 DQ-LTR3-positive haplotypes were preferentially transmitted (84%; P < 10(-6)) compared with 1 of 6 DR-DQ matched DQ-LTR3 negative haplotypes. DQ-LTR3 is missing on most DQB1*0201 haplotypes, and those LTR3 negative haplotypes were also preferentially transmitted to patients (80%; P < 10(-6)), whereas DQB1*0201 DQ-LTR3-positive haplotypes were less often transmitted to patients (36%). Other DQA1/B1 haplotypes did not differ for DQ-LTR3 between transmitted and nontransmitted haplotypes. Thus, the presence of DQLTR3 on HLA DQB1*0302 and its absence on DQB1*0201 haplotypes are independent genetic risk markers for type 1 diabetes.
Published: 1999
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9. Genetic Structure of IDDM1: Two Separate Regions in the Major Histocompatibility Complex Contribute to Susceptibility or Protection

Author: B. Van der Auwera, F. K. Gorus, Frans Schuit, Albert Naipal, Marius J. Giphart, Bart O. Roep, P. De Knijf, and Payman Hanifi Moghaddam
Subjects: Genetics, Linkage disequilibrium, endocrine system diseases, Endocrinology, Diabetes and Metabolism, Haplotype, nutritional and metabolic diseases, Locus (genetics), Human leukocyte antigen, Biology, Major histocompatibility complex, Genetic determinism, immune system diseases, Genotype, Internal Medicine, biology.protein, Microsatellite
Abstract: We analyzed 11 markers in the IDDM1 region in 120 IDDM patients and 83 healthy control subjects who were fully matched for the highest risk HLADQA1*O3O1-DQB1*O3O2/DQA1*O5O1-DQB1*O2O1 genotype. Our study provides strong evidence that two regions in the major histocompatibility complex contribute to IDDM susceptibility or protection. First, despite selection for highest IDDM-associated risk DQ genotypes, this region displays extensive linkage disequilibrium (LD) differences between IDDM patients and control subjects. A second critical region was mapped around the microsatellite locus D6S273 centromeric of TNF, and it is ∼200 kb in size. LD analysis shows that “diabetogenic haplotypes” may have resulted from a recombination telomeric of D6S1014 in the region of D6S273 and TNFa. Haplotype analysis using HLA and microsatellite loci refines IDDM risk assessment in carriers of the HLA-DQ highest risk genotype.
Published: 1998
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10. Effect of Interferon-γ and Glucose on Major Histocompatibility Complex Class I and Class II Expression by Pancreatic β- and Non-β-Cells1

Author: Dejan Pavlovic, Meng-Chi Chen, B. Van der Auwera, Luc Bouwens, Frans Schuit, M. Van De Winkel, and Daniel Pipeleers
Subjects: medicine.medical_specialty, MHC class II, biology, CD74, Antigen processing, Endocrinology, Diabetes and Metabolism, Biochemistry (medical), Clinical Biochemistry, CD1, C-C chemokine receptor type 7, MHC restriction, Biochemistry, Endocrinology, Internal medicine, MHC class I, medicine, biology.protein, CD8
Abstract: Surface major histocompatibility complex (MHC) class I and class II expression by pancreatic islet cells is considered a local initiator or regulator of immune processes that can lead to diabetes. Locally released cytokines, in particular interferon-gamma, are known to stimulate MHC antigen expression by islet cells. The present study quantifies MHC expression in cultured pancreatic beta- and non-beta-cells from both rat and human organs. Interferon-gamma increased MHC class I expression in endocrine beta- and non-beta-cells as well as in pancreatic ductal cells. The cytokine induced a 6-fold increase in the MHC class I messenger ribonucleic acid levels in pancreatic beta-cells; this effect was 2-fold amplified in the presence of elevated glucose levels (20 mmol/L instead of 6 mmol/L). No MHC class II expression was observed in endocrine beta- or non-beta-cells; human, but not rat, ductal cells exhibited MHC class II expression that increased in the presence of interferon-gamma. These data indicate that the increase in beta-cell MHC class I expression described in the pancreata of diabetic patients may result from stimulated transcription after exposure to locally released interferon-gamma and/or to a hyperglycemic state. The association of human islets with ductal cells in which MHC class II expression is stimulated by interferon-gamma makes these cells potential participants in the autoimmune process in diabetes.
Published: 1997
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11. The CTLA-4 gene region of chromosome 2q33 is linked to, and associated with, type 1 diabetes. Belgian Diabetes Registry

Author: Stephen C. Bain, Lorenza Nisticò, Paolo Pozzilli, Emanuele Bosi, Frans Gorus, M S Rios, Frans Schuit, Raffaella Buzzetti, Roberto Tosi, K. H. Jacobs, Clive S. Cockram, L E Pritchard, A. H. Barnett, C. C. Chow, María Teresa Martínez Larrad, B. Van der Auwera, C L Vandewalle, Catherine H. Mijovic, C Giovannini, and John A. Todd
Subjects: Candidate gene, Immunoconjugates, Genetic Linkage, T cell, Biology, Major histocompatibility complex, Nuclear Family, Abatacept, Antigens, CD, Genetic linkage, Genetics, medicine, Humans, Point Mutation, Cytotoxic T cell, CTLA-4 Antigen, Genetic Predisposition to Disease, Molecular Biology, Genetics (clinical), Type 1 diabetes, Polymorphism, Genetic, Exons, General Medicine, medicine.disease, Antigens, Differentiation, Graves Disease, Diabetes Mellitus, Type 1, medicine.anatomical_structure, CTLA-4, Case-Control Studies, Chromosomes, Human, Pair 2, biology.protein, TCF7L2
Abstract: Susceptibility to autoimmune insulin-dependent (type 1) diabetes mellitus is determined by a combination of environmental and genetic factors, which include variation in MHC genes on chromosome 6p21 (IDDM1) and the insulin gene on chromosome 11p15 (IDDM2). However, linkage to IDDM1 and IDDM2 cannot explain the clustering of type 1 diabetes in families, and a role for other genes is inferred. In the present report we describe linkage and association of type 1 diabetes to the CTLA-4 gene (cytotoxic T lymphocyte associated-4) on chromosome 2q33 (designated IDDM12). CTLA-4 is a strong candidate gene for T cell-mediated autoimmune disease because it encodes a T cell receptor that mediates T cell apoptosis and is a vital negative regulator of T cell activation. In addition, we provide supporting evidence that CTLA-4 is associated with susceptibility to Graves' disease, another organ-specific autoimmune disease.
Published: 1996
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12. DRB10403 protects against IDDM in Caucasians with the high-risk heterozygous DQA10301-DQB10302/DQA10501-DQB1*0201 genotype. Belgian Diabetes Registry

Author: B. Van der Auwera, C. Van Waeyenberge, F. Schuit, H. Heimberg, C. Vandewalle, F. Gorus, and J. Flament
Subjects: Endocrinology, Diabetes and Metabolism, Internal Medicine
Published: 1995
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13. Validation of an enzyme-linked immunosorbent assay for C-peptide analysis in Cameroon

Author: Jean Claude Mbanya, Katrijn Verhaeghen, C. Van Schravendijk, F. van Genderen, M. Asanghanwa, B. Van der Auwera, and Eugene Sobngwi
Subjects: Male, Correlation coefficient, Bilirubin, Endocrinology, Diabetes and Metabolism, Reference range, Enzyme-Linked Immunosorbent Assay, Cross Reactions, chemistry.chemical_compound, Endocrinology, Limit of Detection, Reference Values, Poverty Areas, Materials Testing, Internal Medicine, Medicine, Electrochemiluminescence, Humans, Cameroon, Proinsulin, Detection limit, Chromatography, C-Peptide, business.industry, C-peptide, Protein Stability, Reproducibility of Results, General Medicine, chemistry, Biochemistry, Female, Hemoglobin, business
Abstract: To validate an ELISA method for C-peptide analysis in Cameroon.We evaluated the linearity, detection limit, functional sensitivity, precision and accuracy, and further investigated for cross-reactivity by proinsulin, and interferences by lipids, bilirubin and hemoglobin. This method was compared with the Roche electrochemiluminescence immunoassay. C-peptide stability was assessed following a series of freeze-thaw cycles, and after storage at room temperature. The C-peptide reference range was determined by analyzing fifty plasma samples of Cameroonians without diabetes.The ELISA was linear at least up to 7.09 μg/L, and had a detection limit of 0.09 μg/L, and a functional sensitivity of 0.32 μg/L. The inter- and intraassay %CV were 2.9-9.9%, and 5.2-9.4%, respectively. Recoveries were 81-94% in serum, and 93-98% in buffer. Comparison with the ECLIA yielded a good correlation coefficient (R(2)=0.98). There was no cross-reactivity with proinsulin, and no interference with lipids, bilirubin and hemoglobin. C-peptide was stable at room temperature for 24 h and up to 7 freeze-thaw cycles for medium (1-6 μg/L) and high (6 μg/L) levels (-15°C and-70°C). The reference range for C-peptide was 0.38-3.63 μg/L.This method is suitable for C-peptide analysis in low-income countries like Cameroon.
Published: 2012

14. 5' insulin gene polymorphism confers risk to IDDM independently of HLA class II susceptibility

Author: A F Schrevens, J Flament, C van Waeyenberge, Harry Heimberg, B. Van der Auwera, and Frans Schuit
Subjects: Adult, Male, Adolescent, Genotype, Endocrinology, Diabetes and Metabolism, Population, Human leukocyte antigen, Biology, HLA-DQ Antigens, Genetic predisposition, Internal Medicine, Humans, Insulin, Genetic Predisposition to Disease, education, HLA Complex, Aged, Genetics, education.field_of_study, HLA-D Antigens, Polymorphism, Genetic, HLA-DQ Antigen, Haplotype, HLA-DR Antigens, Middle Aged, Variable number tandem repeat, Diabetes Mellitus, Type 1, Phenotype, Immunology, Female
Abstract: The polymorphic variable number of tandem repeats in the 5′ upstream region of the human insulin gene is a well-known non-human leukocyte antigen locus contributing to genetic susceptibility to IDDM. Controversy exists about the question as to whether INS susceptibility haplotypes are or are not preferentially inherited together with HLA-DR4 haplotypes. We investigated whether genetic interaction between INS and the HLA complex can be better defined using DQ genotypic and phenotypic markers in addition to DR serology. The 5′ INS 1/1 genotype was positively associated with IDDM both in non-DR4 subjects (relative risk = 4.3; 95% confidence interval, 1.6–11.5) and DR4 subjects (relative risk = 4.2; 95% confidence interval, 1.9–9.0). Further subdivision of IDDM patients and matched control subjects according to HLA-DQA1 and HLA-DQB1 genotype or phenotype also failed to show any association between 5′ INS and HLA class II genes in diabetic patients. The 5′ INS and HLA class II polymorphisms therefore provide independent risk markers, which may both contribute to the genetic screening of a high-risk population among nondiabetic individuals.
Published: 1993
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15. Aldosterone-secreting adrenal adenoma as part of multiple endocrine neoplasia type 1 (MEN1): loss of heterozygosity for polymorphic chromosome 11 deoxyribonucleic acid markers, including the MEN1 locus

Author: B van der Auwera, K Kovacs, Michel Reznik, P. J. Willems, Achille Stevenaert, Albert Beckers, and R. Abs
Subjects: Adenoma, Genetic Markers, Heterozygote, endocrine system, medicine.medical_specialty, endocrine system diseases, Endocrinology, Diabetes and Metabolism, Clinical Biochemistry, Adrenal Gland Neoplasms, Biology, Biochemistry, Adrenocortical adenoma, Loss of heterozygosity, Endocrinology, Endocrine Glands, Internal medicine, Endocrine Gland Neoplasms, medicine, Humans, Adrenal adenoma, MEN1, Multiple endocrine neoplasia, Aldosterone, Parathyroid adenoma, Polymorphism, Genetic, Chromosomes, Human, Pair 11, Biochemistry (medical), Chromosome Mapping, Syndrome, Middle Aged, medicine.disease, Hyperaldosteronism, Cancer research, Female
Abstract: A 63-year-old female presented with the extremely rare occurrence of an aldosterone-secreting adrenocortical adenoma as part of the syndrome of multiple endocrine neoplasia type 1 (MEN1). Only two other MEN1 patients were reported in the literature with hyperaldosteronism. The patient's MEN1 syndrome consisted of the association of primary hyperparathyroidism due to parathyroid adenoma, a prolactinoma, and a toxic multinodular goiter. Elevated basal and meal-stimulated serum PP levels without demonstrable pancreatic tumor were also found. Genetic analysis of the aldosterone-secreting adenoma with DNA markers localized on chromosome 11 showed loss of heterozygosity in tumor DNA. Since the MEN1 syndrome is caused by loss of the tumor suppressor gene on chromosome 11 in the 11q13 region, it is probable that the same mechanism is associated with the formation of the adrenocortical adenoma.
Published: 1992
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16. Mutational analysis of SRY: nonsense and missense mutations in XY sex reversal

Author: B. Van der Auwera, A. Taylor, J. Levilliers, P. Berta, J. R. Hawkins, and Peter N. Goodfellow
Subjects: Sex Determination Analysis, X Chromosome, Molecular Sequence Data, Restriction Mapping, Nonsense mutation, Disorders of Sex Development, Biology, medicine.disease_cause, Y chromosome, Polymerase Chain Reaction, Y Chromosome, Genetics, medicine, Humans, Missense mutation, Codon, Genetics (clinical), X chromosome, Gonadal Dysgenesis, 46,XY, Mutation, Polymorphism, Genetic, Base Sequence, High Mobility Group Proteins, Tryptophan, Genetic Variation, Nuclear Proteins, Molecular biology, Sex-Determining Region Y Protein, Stop codon, DNA-Binding Proteins, High-mobility group, Testis determining factor, Oligodeoxyribonucleotides, Female, Transcription Factors
Abstract: XY females (n = 17) were analysed for mutations in SRY (sex-determining region Y gene), a gene that has recently been equated with the testis determining factor (TDF). SRY sequences were amplified by the polymerase chain reaction (PCR) and analysed by both the single strand conformational polymorphism assay (SSCP) and DNA sequencing. The DNA from two individuals gave altered SSCP patterns; only these two individuals showed any DNA sequence variation. In both cases, a single base change was found, one altering a tryptophan codon to a stop codon, the other causing a glycine to arginine amino acid substitution. These substitutions lie in the high mobility group (HMG)-related box of the SRY protein, a potential DNA-binding domain. The corresponding regions of DNA from the father of one individual and the paternal uncle of the other, were sequenced and found to be normal. Thus, in both cases, sex reversal is associated with de novo mutations in SRY. Combining this data with two previously published reports, a total of 40 XY females have now been analysed for mutations in SRY. The number of de novo mutations in SRY is now doubled to four, adding further strength to the argument that SRY is TDF.
Published: 1992
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17. Association of KIR2DL2 polymorphism rs2756923 with type 1 diabetes and preliminary evidence for lack of inhibition through HLA-C1 ligand binding

Author: F. Scholten, C. Seidl, B. Van der Auwera, Folefac Aminkeng, C. Wild, Klaus Badenhoop, Elizabeth Ramos-Lopez, H. Kalhes, T. Tonn, Diabetes Pathology & Therapy, and Medical Biochemistry
Subjects: Cytotoxicity, Immunologic, Male, Genotype, type 1 diabetes, Immunology, Killer-cell immunoglobulin-like receptor, Human leukocyte antigen, HLA-C Antigens, Biology, Biochemistry, Polymorphism, Single Nucleotide, polymorphism, Exon, Belgium, Gene Frequency, Cell Line, Tumor, Germany, Gene cluster, Genetics, medicine, Immunology and Allergy, Humans, Genetic Predisposition to Disease, Allele, Receptor, Alleles, Type 1 diabetes, Haplotype, General Medicine, medicine.disease, Molecular biology, Killer Cells, Natural, Diabetes Mellitus, Type 1, Haplotypes, Receptors, KIR2DL2, killer cell immunoglobulin-like receptor, Female
Abstract: Killer cell immunoglobulin-like receptors (KIRs) on chromosome 19q13.4 regulate the function of not only human natural killer (NK) cells but also T cells. An increase in activating KIR- human leucocyte antigen ligand pairs has been associated with an additional risk to develop type 1 diabetes (T1D). T1D families [n = 184 (552 individuals); n = 176 (528 subjects)], unrelated T1D patients (n = 380; n = 394) and healthy controls (n = 315; n = 401) from Germany and Belgium, respectively, were genotyped for the rs2756923 polymorphism within the KIR gene cluster haplotype B in exon 8 of the KIR2DL2 gene. We observed in both Germans and Belgians an overtransmission of the allele 'G' of the KIR2DL2-rs2756923 polymorphism (64.2% vs 35.8%, P = 3 x 10(-4) and 60.0% vs 40.0%, P = 0.02, respectively). In addition, this allele was more frequent in German patients than in healthy controls (78.4% vs 21.6%, P = 1 x 10(-3)). Preliminary results from a cytotoxicity assay suggest that inhibition of NK-cell cytotoxicity may be impaired in individuals carrying the rs2756923 G allele. These data suggest a potential role of the KIR2DL2-rs2756923 polymorphism in T1D in Germans and Belgians.
Published: 2009

18. Combined positivity for HLA DQ2/DQ8 and IA-2 antibodies defines population at high risk of developing type 1 diabetes

Author: I. Truyen, F. K. Gorus, Bart Keymeulen, Daniel Pipeleers, Chantal Mathieu, K. Decochez, Belgian Diabetes Registry, B. Van der Auwera, I. De Leeuw, E. Vandemeulebroucke, R. Rottiers, I Weets, Belgian Diabet Registry, Medical Biochemistry, Vrije Universiteit Brussel, and Pathologic Biochemistry and Physiology
Subjects: Male, Time Factors, type 1 diabetes, Insulin Antibodies, Endocrinology, Diabetes and Metabolism, Carbon-carbon lyases, Endocrinopathy, Autoimmunity, Pancreatic hormone, Autoantibody, Risk Factors, Immunopathology, Autoimmune disease, Insulin, Prospective Studies, Child, education.field_of_study, Glutamate Decarboxylase, HLA-DQ2, HLA-System, Disease Progression, Regression Analysis, Female, Adult, Carboxy-lyases, Adolescent, Genotype, Population, Lyases, Biology, Disease-Free Survival, Langerhans islet, HLA-DQ Antigens, Diabetes mellitus, HLA-DQ, Internal Medicine, medicine, Humans, Family, Endocrine pancreas, Risk factor, First-degree relatives, education, development, Antibody, Autoantibodies, Family Health, Type 1 diabetes, Prevention, medicine.disease, Diabetes Mellitus, Type 1, Haplotypes, Enzyme, Immunology, Human medicine, Prediction
Abstract: Aims/hypothesis: Prevention trials in first-degree relatives of type 1 diabetic patients are hampered by large interindividual differences in progression rate to diabetes. We investigated whether specific combinations of immune and genetic markers can identify subgroups with more homogeneous progression to clinical onset. Methods: Antibodies against islet cell cytoplasm (ICA), insulin (IAA), glutamate decarboxylase (GADA) and IA-2 protein (IA2A) were measured in 790 non-diabetic control subjects and 4,589 first-degree relatives under age 40. Results: On first sampling, 11.1% of the siblings presented at least one antibody type ( p< 0.001 vs other relatives). During follow-up ( median 52 months) 43 subjects developed type 1 diabetes ( 31 siblings, ten offspring of a diabetic father, two offspring of a diabetic mother). Using Kaplan - Meier survival analysis and Cox regression, IA-2A conferred the highest 5-year diabetes risk (> 50%) irrespective of the number of antibodies present. In initially IA-2A-positive relatives (n = 58) progression to hyperglycaemia depended more on HLA DQ status than on type of kinship (84% progression in the presence of DQ2/DQ8 vs 32% in its absence; p< 0.003). In IA-2A-negative relatives (n = 4,531) 5-year progression to diabetes increased with the number of other antibodies (ICA, GADA and/or IAA) ( p< 0.001) but overall did not exceed 10% even for two or more antibodies. Among relatives initially positive for one or more antibody type other than IA-2A (n = 315), there was significantly more progression to diabetes ( overall still < 10%) in carriers of DQ2 ( p< 0.001 vs no DQ2), regardless of DQ8 status. Conclusions/interpretation: These observations suggest that the HLA-DQ-inferred risk of diabetes can proceed through two distinct pathways distinguished by IA-2A status. Combined positivity for DQ2/DQ8 and IA-2A defines a more homogeneous high-risk population for prevention trials than those used so far.
Published: 2005

19. 40(th) EASD Annual Meeting of the European Association for the Study of Diabetes : Munich, Germany, 5-9 September 2004

Author: S. Artigas, A V Dreval, Mark I. McCarthy, C Watson, Peter H. Bennett, M Quint, Y Ikeda, E Alpert, F Schiele, H Sekihara, Erik Gylfe, P Lowe, J Kuhlmann, Alain Golay, V Longo, Shahidul Alam Khan Akm., L G Mantovani, M Zawodniak-Szalapska, G Winkler, T Harrity, L Virág, U Johne, Kuo S-W., Linda C Tapsell, J Rodriguez, Michel Komajda, K Kankova, Carole A. Cull, M Sporna, E Estilles, U Ribel, M C Spruce, E Buzzigoli, T Prazak, J K McLaughlin, M K Lingohr, M Lim, F Calara, A Siebenhofer, G Meregalli, Roberto Anichini, A D Baron, R Kurashvili, P C Butler, G I Fantus, T. E. De Gooyer, Park Y-M., R. Walther, S Heinrich, Agnieszka Zawiejska, S Mukherjee, Nikolaos Papanas, G Wong, Ian D. Caterson, David M. Maahs, Shuichi Kaneko, Alexandra E. Butler, Francisco Javier Ampudia-Blasco, O N Kong, Attali J-R., C A Hedman, K Oshinyemi, Nicolle Müller, I C Cranston, N Okumus, M V Vlaiculescu, Balasubramanian Ravikumar, W W Cheatham, K Mukasa, K B Biswas, Annunziata Lapolla, Phil McEwan, G Mader, Gilles Chassot, Dragi Anevski, Werner A. Scherbaum, M Donath, C Hesselmann, R A Gandhi, David E. Moller, Ezio Bonifacio, C Garcia, V Ifandi, P Hornnes, Nieuwenhoven Fav., C Puech, S Pérez-Del-Pulgar, Kim S-R., G Hines, C Rubio Terrés, Michael Gaster, N. Hosszufalusi, A Scholze, Andrew A. Young, Stavros Liatis, F Hariri, S Tan, Paul Valensi, Allan E. Karlsen, J Kim, E. Moberg, J Kaiser, L Berman, G Nelson, A Altkrüger, P Kothare, D B Cook, S Doran, G. van Dijk, Shahnaz Shahinfar, Kim C-S., P Stahl, M Manousaki, S Sigrist, S K Lim, M. P. Stern, A Guberti, C Rezzani, J McKenney, Karl Thomaseth, Sofia Carlsson, M Julia, R Brillante, I Rubesova, T Darkow, E Matsumoto, Wendy M. Macfarlane, M Di Martino, G Bardini, Rossella Menghini, D Duhot, E Farcasiu, Annalisa Natalicchio, I Lindner, J Buvat, Christian L. Brand, Harry Dorchy, Iwona Pietrzak, Z T Luo, P Home, M Ekelund, Jesper Gromada, Kristine Færch, F Piarulli, H Kim, R Mentel, Zsuzsanna K. Zsengellér, Dullaart Rpf., Anton Luger, Thomas A. Pearson, V Manicardi, P Rösen, Feng Y-M., R Morganti, Lars Hansen, Demuth H-U., Haruo Kasai, A Shostak, Rudi Steffensen, G Taylor, Markolf Hanefeld, C Santini, E Hamaguchi, Roberto Miccoli, F Storms, M Cooper, Y Lee, Allison E. Aiello, P Smith, T Suehiro, K Treece, M Waluś, Timothy A Welborn, Simone Baltrusch, E Kontela, S Chai, J Crean, H Yokoyama, Johan G. Eriksson, Rafael Hernández Hernández, J Rodríguez-Saldaña, M P Tornero, G Formoso, D. Lovell, E Bingham, A Mylonakis, M Manteghetti, D Fedele, Antonio Martín-Duce, Ralph A. DeFronzo, D Salcedo, Kurt Højlund, Antonio Petrone, Sheu Whh., C Gutierrez, Flavia Pricci, S Kurita, Z G Abbas, M M Benedetti, Philippe A. Halban, Daniel J. Cox, O Ljungkvist, Justine Davies, J Palsgaard, Lars Sjöström, E Bosi, L Janin-Manificat, W. F. Kelly, M. Fernandez, E Colak, O V Mulyarchik, B Kronshage, F Lang, M Erfurth, Takashi Kadowaki, N Jendrike, U Walter, J Wishart, Y. Neye, D Kim, N Furuhashi, M Barsotti, D Florow, L Ke, L Borgquist, N C Jackson, Ffolliott M. Fisher, V Baskar, K Yoshioka, Bryan A. Wolf, G Chabrier, R Skoumal, Livio Luzi, H Kose, I Pharisien, B. Klein, H Winiarska, M C Johnson, L Griffiths, Nonna Kravchun, C Combe, Baptist Gallwitz, J Zdychova, L Skorda, Jorma Ilonen, W Gao, I N Steen, A Terrinoni, P D Ambery, W Kern, C M Kusminski, Cho M-H., Paolo Pozzilli, Louise G. Grunnet, E Schönle, David R Matthews, Robert W. Taylor, Y Cohen, Kim H-S., M P Eccles, N B Tutuncu, D McDowell, Richard M. Bergenstal, K Takamatsu, T Steiner, Jaan Palgi, Valdemar Grill, N Niculescu, G Federici, S Lehto, P. M. McKeigue, M Barone, Michael E. Trautmann, S Smirnov, J Mannion, M Eto, C Rousseau, M Conti, C S Ernest, Antonio Ceriello, D H Schweitzer, Jung E-D., Andreas Festa, Avijit Lahiri, A Shepelkevich, A Murro, A Kollmann, Jonathan R.S. Arch, R Landgraf, Son H-Y., I Engelsberger, E Agardh, S Rodríguez-Mulero, P J Kraml, K Lee, D. F. Du Toit, E Kim, G Fadini, Williams Ajk., Philip Home, M B Antcieferov, C Perlemoine, D Perrea, Song X-L., D Ruggieri, Krister Bokvist, Heidi Sørensen, Bilbao, G Yoshino, J P Taylor, Shen H-M., S M Furier, R Urquhart, J Wohlgelernter, Jianping Weng, T. Baba, Q Hong, C Silva, Castaigne J-P., M Felaco, X X Zhang, M Jaroň, Milla Rosengård-Bärlund, J G Papp, Toshio Miyata, Lervang H-H., Park M-K., I Kinalska, A Long, Oomen Phn., N Kogawa, Ippolita Patrizia Patera, S. Karadeniz, Dinesh Selvarajah, D S Chung, A Wensaas, Richard Imrich, M Recasens, J Ruxer, O Buchea, E Wilpart, S P Stepanenko, Le Ttd., H Ohgawara, Mariaconsuelo Valentini, A Mondok, M Peltonen, Marianne O. 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Jensen, G, Fisher, A, Petrovsky, N, Srikusalanukul, W, Budge, M, Trifunovic zamaklar, D, Zivkovic, M, Jelic, V, Vukomanovic, G, Ristic, A, Seferovic, P, Costa, J, Duarte, S, Manley, S, Sailesh, S, Venkataraman, A, Haider, Y, Groza, I, Oprean, M, Ardelean, A, Morosanu, A, Darkow, T, Vanderplas, A, Mamas, M, Mcelduff, P, Burns, J, Edwards, R, Fitchet, A, Young, R, Gibson, J, Lichiardopol, R, Niculescu, N, Totora, A, Pencea, C, Tomescu, I, Cinteza, M, Manicardi, V, Coscelli, C, Navazio, A, Catellani, E, Michelini, M, Dall'Asta, D, Guberti, A, Piazza, A, Gasparini, E, Pantaleoni, M, Guiducci, U, Manari, A, Sejil, S, Janand delenne, B, Avierinos, J, Habib, G, Labastie, N, Vague, P, Lassmann vague, V, Luźniak, P, Tatoń, J, Wojciechowska Luźniak, A, Zairis, M, Lyras, A, Patsourakos, N, Tsirimbis, V, Foussas, S, Lupón, J, Urrutia, A, Herreros, J, González, B, Coll, R, Altimir, S, Prats, M, Valle, V, Abreu padí, C, Rábago, G, Ivanova, L, Brasacchio, D, Harno, E, Keenan, A, Li, H, Lu, Z, Ke, L, Liu, H, Jeong, I, Chae, M, Choi, M, Yoo, H, Kim, C, Yun, M, Na, M, Kang, Y, Kong, O, Son, S, Kim, I, Tanaka, N, Hosoi, M, Matsuyama, Y, Fukumoto, M, Yamakita, T, Yoshioka, K, Ishii, T, Sato, T, Fujii, S, Aoki, T, Shibata, T, Mizutani, N, Suzuki, J, Fowelin, J, Samuelsson, P, Brandrup wogsen, G, Okumura, K, Tokmakova, A, Staroverova, D, Antcieferov, M, Shutichina, I, Kuntchevich, G, Vriesendorp, T, Morélis, Q, Legemate, D, Schaper, F, Mainas, E, Gkioulmpasanis, I, Panagiotou, I, Vassilikos, G, Skorda, L, Sidira, M, Christoforidou, M, Alaveras, A, Artikis, V, Evdemon, E, Lechleitner, M, Koch, T, Ebenbichler, C, Sturm, W, Moretti, L, Moruzzo, D, Boldrini, E, Pandolfo, C, Kameyama, M, Iwasa, R, Cho, M, Nam, J, Huh, K, Kaplar, M, Paragh, G, Erdei, A, Csongradi, E, Garai, I, Varga, J, Galuska, L, Udvardy, M, Higa, M, Kaneko, Y, Hiroi, N, Koziarska, D, Nowacki, P, Majkowska, L, Luzniak, P, Wojciechowska luźniak, A, Tushuizen, M, Nieuwland, R, Snoeck, D, Sturk, A, Diamant, M, Aguiar, L, Bahia, L, Villela, N, Laflor, C, Conde, C, Bottino, D, Dorigo, D, Bouskela, E, Pu, S, Luo, Z, Lam, K, Dan, Q, Xu, A, Shen, J, Cheng, K, Xu, J, Thamer, C, Stefan, N, Haap, M, Heller, E, Tschritter, O, De Prado, A, Ortiz, A, Ybarra, J, Gich, I, Pou, J, Ehren, M, Roggenland, D, Reinsen, B, Klein, H, Rittig, K, Stock, J, Kocher, B, Balletshofer, B, Shon, H, Chung, D, Nakatani, Y, Matsuhisa, M, Kaneto, H, Hatazaki, M, Yoshiuchi, K, Katakami, N, Kawamori, D, Ohtoshi, K, Sakamoto, K, Matsuoka, T, Ozawa, K, Ogawa, S, Hori, M, Yamasaki, Y, Zitouni, K, Harry, D, Nourooz zadeh, J, Earle, K, Olesen, P, Franco, L, Corvaja, C, Semplicini, A, Ceylan işık, A, Arı, N, Rösen, P, Lee, I, Park, K, Jung, E, Shin, D, Jo, S, Obuobie, K, Prakash, P, Hanna, F, Lazarus, J, Varadhan, L, Gurushankar, J, James, D, Sheikh, S, Gaede, P, Zou, D, Vilarrasa, N, Perez maraver, M, Mena, E, Perez, D, Setti, G, Buckingham, R, Urbančič, V, Stefanovska, A, Bernjak, A, Ažman juvan, K, Kocijančič, A, Glowania, A, Filters, T, Fosmark, D, Torjesen, P, Kilhovd, B, Berg, T, Sandvik, L, Hanssen, K, Mentink, C, Donchenko, G, Stepanenko, S, Maingrette, F, Deng, H, Lindenmair, A, Freudenthaler, A, Baumgartner parzer, S, Nizheradze, K, Khoruzhenko, A, Tronko, N, Sheu, W, Ou, H, Shen, H, Lin, T, Wu, H, Yang, C, Mogylnytska, L, Schmoelzer, I, Davies, J, Band, M, Struthers, A, Prázný, M, Škrha, J, Kasalová, Z, Neelotpol, S, Jahan, P, Kauschke, S, Harrop, C, Schäfer, A, Widder, J, Eigenthaler, M, Walter, U, Uchimura, I, Ikebukuro, M, Kaibara, M, Hirata, M, Helal, R, Pervin, F, Yang, X, Jansson, P, Nagaev, I, Jack, M, Carvalho, E, Sunnerhagen, K, Cam, M, Cushman, S, Smith, U, Creely, S, Farmer, J, Gustafson, B, Kusminski, C, Krusinova, E, Wohl, P, Klementova, M, Lanska, V, Mcdougall, C, Kelly, I, Abbas, Z, Lutale, J, Archibald, L, Karunajeewa, H, Stingemore, N, Stuccio, G, Mcgechie, D, Muller, L, Hak, E, Goudzwaard, W, Montorsi, F, Homering, M, Sprenger, K, Goldstein, I, Asnaghi, V, Ferrari, G, Rastaldi, M, Gabellini, D, Dell'Antonio, G, Maestroni, A, Ruggieri, D, Luzi, L, Piemonti, L, Zerbini, G, Anafaroglu, I, Tutuncu, N, Sultana, M, Siddiqua, N, Iwasaki, T, Nakajima, A, Yoneda, M, Mukasa, K, Tanaka, S, and Sekihara, H
Subjects: 0303 health sciences, medicine.medical_specialty, business.industry, EASD, Endocrinology, Diabetes and Metabolism, Human physiology, medicine.disease, 03 medical and health sciences, 0302 clinical medicine, Diabetes mellitus, Family medicine, Internal Medicine, Medicine, business, 030217 neurology & neurosurgery, 030304 developmental biology
Published: 2004

20. The association of astrocytoma and pituitary adenoma in a patient with alcaptonuria

Author: J. J. Martin, P. J. Willems, E Van de Kelft, E. Van Marck, B. Van der Auwera, Albert Beckers, Roger Abs, M. Van Vyve, I. Neetens, and E. Van den Ende
Subjects: Adenoma, Adult, Pathology, medicine.medical_specialty, Astrocytoma, Biology, Pituitary neoplasm, Alkaptonuria, Neoplasms, Multiple Primary, Pituitary adenoma, Female patient, medicine, Humans, Genes, Tumor Suppressor, Genetic Predisposition to Disease, Pituitary Neoplasms, Genes tumor suppressor, Brain Neoplasms, Juvenile Pilocytic Astrocytoma, medicine.disease, Cranial Fossa, Posterior, Neurology, Inborn error of metabolism, Female, Neurology (clinical)
Abstract: A female patient with a juvenile pilocytic astrocytoma and a pituitary adenoma is described. The patient also has alcaptonuria, a rare inborn error of metabolism with autosomal recessive mode of inheritance. The association of these three disorders has never been reported previously. The possible existence of a common genetic factor in the development of both tumors and alcaptonuria is discussed.
Published: 1992
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21. HLA-DRB1*04 and susceptibility to type 1 diabetes mellitus in a German/Belgian family and German case-control study. The Belgian Diabetes Registry

Author: H, Donner, C, Seidl, B, Van der Auwera, J, Braun, T, Siegmund, J, Herwig, I, Weets, K H, Usadel, and K, Badenhoop
Subjects: Adult, Male, Adolescent, Infant, HLA-DR Antigens, HLA-DQ alpha-Chains, Diabetes Mellitus, Type 1, Belgium, Case-Control Studies, Child, Preschool, Germany, HLA-DQ Antigens, HLA-DQ beta-Chains, Humans, Female, Genetic Predisposition to Disease, Disease Susceptibility, Child, HLA-DRB1 Chains
Abstract: HLA-DR4 is a primary disease association marker in type 1 diabetes mellitus (IDDM). We therefore analyzed the transmission of 228 DR4+ haplotypes in 183 families with an IDDM proband (95 from Germany and 88 from Belgium). In a separate case-control data set, we investigated the HLA-DRB1*04 and DQ allele distribution in 245 IDDM patients and 177 controls from Germany, all DR4 positive. HLA-DRB1 *0401 and *0402 linked to DQB1 *0302 were significantly more often transmitted to patients in the studied families (81% and 89%) in contrast to DRB1 *0401-DQB1 *0301 (33%). The case-control study of HLA-DQB1 *0302+ individuals revealed -DRB1 *0405 to be more frequent in patients with IDDM and HLA-DRB1 *0403 and -DRB1 *0404 to be less frequent. HLA-DQA1 *0102-DQB1 *0602 and -DQA1 *0501-DQB1 *0301 in trans complementation with DRB1 *0401-DQB1 *0302 were also significantly less frequent in IDDM patients (P3x 10(-7) and P0.02). In conclusion, HLA-DRB1 *0403 and -DQB1*0301 alleles in cis as well as protective DQ haplotypes in trans, confer dominant protection against IDDM in a German / Belgian population.
Published: 2000

22. The presence or absence of a retroviral long terminal repeat influences the genetic risk for type 1 diabetes conferred by human leukocyte antigen DQ haplotypes. Belgian Diabetes Registry

Author: H, Donner, R R, Tönjes, B, Van der Auwera, T, Siegmund, J, Braun, I, Weets, J, Herwig, R, Kurth, K H, Usadel, and K, Badenhoop
Subjects: Male, Heterozygote, Diabetes Mellitus, Type 1, Haplotypes, HLA-DQ Antigens, Endogenous Retroviruses, Terminal Repeat Sequences, Humans, Female, Genetic Predisposition to Disease
Abstract: Major genetic susceptibility to type 1 diabetes mellitus maps to the human leukocyte antigen (HLA) region on chromosome 6p. During evolution, endogenous retroviral long terminal repeats (LTR) have been integrated at several sites within this region. We analyzed the presence of a solitary HERV-K LTR in the HLA DQ region (DQ-LTR3) and its linkage to DRB1, DQA1, and DQB1 haplotypes derived from 246 German and Belgian families with a patient suffering from type 1 diabetes mellitus. Segregation analysis of 984 HLA DQA1/B1 haplotypes showed that DQ-LTR3 is linked to distinct DQA1 and DQB1 haplotypes but is absent in others. The presence of DQ-LTR3 on HLA DQB1*0302 haplotypes was preferentially transmitted to patients from heterozygous parents (82%; P10(-6)), in contrast to only 2 of 7 DQB1*0302 haplotypes without DQ-LTR3. Also, the extended HLA DRB1*0401, DQB1*0302 DQ-LTR3-positive haplotypes were preferentially transmitted (84%; P10(-6)) compared with 1 of 6 DR-DQ matched DQ-LTR3 negative haplotypes. DQ-LTR3 is missing on most DQB1*0201 haplotypes, and those LTR3 negative haplotypes were also preferentially transmitted to patients (80%; P10(-6)), whereas DQB1*0201 DQ-LTR3-positive haplotypes were less often transmitted to patients (36%). Other DQA1/B1 haplotypes did not differ for DQ-LTR3 between transmitted and nontransmitted haplotypes. Thus, the presence of DQLTR3 on HLA DQB1*0302 and its absence on DQB1*0201 haplotypes are independent genetic risk markers for type 1 diabetes.
Published: 1999

23. Genetic structure of IDDM1: two separate regions in the major histocompatibility complex contribute to susceptibility or protection. Belgian Diabetes Registry

Author: P, Hanifi Moghaddam, P, de Knijf, B O, Roep, B, Van der Auwera, A, Naipal, F, Gorus, F, Schuit, and M J, Giphart
Subjects: Adult, Genetic Markers, Male, Genotype, Tumor Necrosis Factor-alpha, Polymerase Chain Reaction, HLA-DQ alpha-Chains, Linkage Disequilibrium, Major Histocompatibility Complex, Diabetes Mellitus, Type 1, Gene Frequency, Haplotypes, HLA-DQ Antigens, HLA-DQ beta-Chains, Humans, Female, Alleles, Microsatellite Repeats
Abstract: We analyzed 11 markers in the IDDM1 region in 120 IDDM patients and 83 healthy control subjects who were fully matched for the highest risk HLA-DQA1*0301-DQB1 *0302/DQA1*0501-DQB1*0201 genotype. Our study provides strong evidence that two regions in the major histocompatibility complex contribute to IDDM susceptibility or protection. First, despite selection for highest IDDM-associated risk DQ genotypes, this region displays extensive linkage disequilibrium (LD) differences between IDDM patients and control subjects. A second critical region was mapped around the microsatellite locus D6S273 centromeric of TNF, and it is approximately 200 kb in size. LD analysis shows that "diabetogenic haplotypes" may have resulted from a recombination telomeric of D6S1014 in the region of D6S273 and TNFa. Haplotype analysis using HLA and microsatellite loci refines IDDM risk assessment in carriers of the HLA-DQ highest risk genotype.
Published: 1998

24. CTLA-4 gene polymorphism confers susceptibility to insulin-dependent diabetes mellitus (IDDM) independently from age and from other genetic or immune disease markers

Author: C L Vandewalle, G. Lamberigts, F. K. Gorus, I. De Leeuw, Frans Schuit, S Van Imschoot, B. Van der Auwera, and Frederic Winnock
Subjects: Adult, Male, Immunoconjugates, endocrine system diseases, Editorial Review, Immunology, Human leukocyte antigen, Biology, Abatacept, Antigens, CD, Immunopathology, Genotype, Immunology and Allergy, Humans, CTLA-4 Antigen, Genetic Predisposition to Disease, Allele, Child, Autoantibodies, Polymorphism, Genetic, Haplotype, Autoantibody, Age Factors, Infant, Antigens, Differentiation, Variable number tandem repeat, Diabetes Mellitus, Type 1, Genetic marker, Child, Preschool, Female, Biomarkers
Abstract: SUMMARY Apart from genes in the HLA complex (IDDM1) and the variable number of tandem repeats in the 5′ region of the insulin gene (INS VNTR, IDDM2), several other loci have been proposed to contribute to IDDM susceptibility. Recently, linkage and association have been shown between the cytotoxic T lymphocyte-associated protein 4 (CTLA-4) gene on chromosome 2q and IDDM. In a registry-based group of 525 recent-onset IDDM patients
Published: 1997

25. TNFa microsatellite polymorphism modulates the risk of IDDM in Caucasians with the high-risk genotype HLA DQA10501-DQB10201/DQA10301-DQB10302. Belgian Diabetes Registry

Author: P H, Moghaddam, A H, Zwinderman, P, de Knijff, B O, Roep, R F, Schipper, B, Van der Auwera, A, Naipal, F, Gorus, F, Schuit, and M J, Giphart
Subjects: Diabetes Mellitus, Type 1, Polymorphism, Genetic, Haplotypes, Risk Factors, Tumor Necrosis Factor-alpha, HLA-DQ Antigens, HLA-DQ beta-Chains, Humans, Epistasis, Genetic, HLA-DQ alpha-Chains, Microsatellite Repeats
Published: 1997

26. Proinsulin and its conversion intermediates in human pancreas and isolated islet tissue: kinetics and steady-state analysis

Author: Andre Foriers, Paule Houssa, C. Van Schravendijk, Y. Zambre, J. C. Sodoyez, Michelle Deberg, Zhidong Ling, C. N. Hales, Daniel Pipeleers, X. Hou, and B. Van der Auwera
Subjects: Adult, Male, endocrine system, medicine.medical_specialty, endocrine system diseases, Adolescent, medicine.drug_class, Endocrinology, Diabetes and Metabolism, medicine.medical_treatment, Prohormone, Peptide, Biology, Tritium, Islets of Langerhans, Endocrinology, Internal medicine, Internal Medicine, medicine, Humans, Protein Precursors, Immunoadsorption, Child, Pancreas, Immunosorbent Techniques, Proinsulin, chemistry.chemical_classification, geography, Immunoradiometric assay, geography.geographical_feature_category, Hepatology, Insulin, Middle Aged, Islet, Sulfonylurea, Tissue Donors, Kinetics, chemistry, Diabetes Mellitus, Type 2, Child, Preschool, Female, hormones, hormone substitutes, and hormone antagonists, medicine.drug
Abstract: In non-insulin-dependent diabetes, circulating insulin-related immunoreactivity (IRI) is often composed of a higher fraction of the incompletely converted forms proinsulin and des-31,32 proinsulin. The present study describes an immunoadsorption method for measuring the proportions of proinsulin, its two split products, and insulin in human pancreatic tissue and for determining their rates of formation in human isolated islets. The method uses two junction-specific monoclonal proinsulin antibodies in a protein G fractionation; it is validated by > or = 90% specificity and recovery. The peptide contents measured in tissue extracts were comparable to those determined in a previously developed immunoradiometric assay. In the nine tissue extracts from nondiabetic donor organs, 97% of IRI corresponded to insulin, 1% to proinsulin, 2% to the des-31,32 proinsulin conversion product, and 0.1% to des-64,65 proinsulin. Two samples from non-insulin-dependent diabetics under sulfonylurea treatment contained a fourfold lower content of IRI but the peptide distribution was comparable except for a low percentage (0.3) of proinsulin in one case. In pulse-chase experiments on three-preparations of human islets isolated from nondiabetic donors, proinsulin represented the major (> 90%) IRI that was synthesized at the end of the 30-min pulse; a subsequent 90-min chase at either 2.5 or 10 mM glucose resulted in conversion of 75% of proinsulin to des-31,32 (20%) and des-64,65 (2%) intermediates and to insulin (50%); after a 180-min chase, 88% of proinsulin was converted to insulin, but 10% remained present as proinsulin. In a pulse-chase experiment on islets isolated from tissue with a high proportion of des-31,32 intermediate (5% instead of 2%), the conversion process was slower (45% after 90 min and 70% after 180 min) and resulted in a higher fraction of des-31,32 intermediate, suggesting that the elevated tissue content in this intermediate is caused by a reduced PC2 converting activity. These data confirm that des-31,32 proinsulin represents the major conversion intermediate in normal human islets and indicate the existence of slow converters, possibly as a result of decreased enzymatic processing of the prohormone's AC junction.
Published: 1997

27. Effect of interferon-gamma and glucose on major histocompatibility complex class I and class II expression by pancreatic beta- and non-beta-cells

Author: D, Pavlovic, M, van de Winkel, B, van der Auwera, M C, Chen, F, Schuit, L, Bouwens, and D, Pipeleers
Subjects: Adult, Male, Adolescent, Histocompatibility Antigens Class I, Histocompatibility Antigens Class II, Middle Aged, Flow Cytometry, Immunohistochemistry, Rats, Interferon-gamma, Islets of Langerhans, Glucose, Animals, Humans, Keratins, Rats, Wistar, Fluorescent Antibody Technique, Indirect, beta 2-Microglobulin, Pancreas
Abstract: Surface major histocompatibility complex (MHC) class I and class II expression by pancreatic islet cells is considered a local initiator or regulator of immune processes that can lead to diabetes. Locally released cytokines, in particular interferon-gamma, are known to stimulate MHC antigen expression by islet cells. The present study quantifies MHC expression in cultured pancreatic beta- and non-beta-cells from both rat and human organs. Interferon-gamma increased MHC class I expression in endocrine beta- and non-beta-cells as well as in pancreatic ductal cells. The cytokine induced a 6-fold increase in the MHC class I messenger ribonucleic acid levels in pancreatic beta-cells; this effect was 2-fold amplified in the presence of elevated glucose levels (20 mmol/L instead of 6 mmol/L). No MHC class II expression was observed in endocrine beta- or non-beta-cells; human, but not rat, ductal cells exhibited MHC class II expression that increased in the presence of interferon-gamma. These data indicate that the increase in beta-cell MHC class I expression described in the pancreata of diabetic patients may result from stimulated transcription after exposure to locally released interferon-gamma and/or to a hyperglycemic state. The association of human islets with ductal cells in which MHC class II expression is stimulated by interferon-gamma makes these cells potential participants in the autoimmune process in diabetes.
Published: 1997

28. Genetic susceptibility for insulin-dependent diabetes mellitus in Caucasians revisited: the importance of diabetes registries in disclosing interactions between HLA-DQ- and insulin gene-linked risk. Belgian Diabetes Registry

Author: F. K. Gorus, Frans Schuit, Alberto Falorni, B. Van der Auwera, C L Vandewalle, S Svanholm, I Lyaruu, Medical Biochemistry, and Pathologic Biochemistry and Physiology
Subjects: Adult, Male, Risk, diabetes registries, Adolescent, Genotype, endocrine system diseases, medicine.medical_treatment, Endocrinology, Diabetes and Metabolism, Clinical Biochemistry, HLA-Dq, Human leukocyte antigen, Biochemistry, White People, Endocrinology, HLA-DQ Antigens, Diabetes mellitus, HLA-DQ, Genetic predisposition, Humans, Insulin, Medicine, Genetic Predisposition to Disease, IDDM, Registries, Age of Onset, Child, Polymorphism, Genetic, HLA-DQ Antigen, business.industry, Biochemistry (medical), Infant, Newborn, Infant, Middle Aged, medicine.disease, Diabetes Mellitus, Type 1, Genes, Child, Preschool, Immunology, Female, Age of onset, business, genetic susceptibility
Abstract: Whether genetic susceptibility for insulin-dependent diabetes mellitus (IDDM) at the 5' insulin gene polymorphic region (5' INS) interacts with human leukocyte antigen (HLA)-DQ-linked disease risk and whether it is associated with autoantibody formation is presently controversial. Diabetes registries allow more systematic reassessment of these questions. Two hundred and ninety-six Caucasian IDDM patients were recruited by the Belgian Diabetes Registry and sampled at disease onset, together with 195 ethnically matched control subjects. 5'INS genotypes were determined by Southern blotting, HLA-DQ by allele-specific oligotyping, and autoantibodies by validated immunoassays. The 5' INS 1/1 genotype was more prevalent in patients than in controls [relative risk (RR) = 2.3; P
Published: 1995

29. DQ-LTR13 modifies Type 1 diabetes (IDDM) susceptibility on high risk DQ haplotypes: reply to the comments of Pascual et al

Author: B. Van der Auwera, C. Seidl, K. Krach, J. Van Autreve, M. A. Pani, F. K. Gorus, Ralf R. Tönjes, and Klaus Badenhoop
Subjects: Genetics, Type 1 diabetes, Endocrinology, Diabetes and Metabolism, Haplotype, Internal Medicine, medicine, Human physiology, Biology, medicine.disease
Published: 2003
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30. Molecular cytogenetic analysis of XX males using Y-specific DNA sequences, including SRY

Author: Ingeborg Liebaers, S Castedo, Franki Speleman, Jan E. Dumon, A. De Paepe, B. Van der Auwera, N. Van Roy, J. R. Hawkins, Medical Biochemistry, and Department of Embryology and Genetics
Subjects: Adult, Male, medicine.medical_specialty, Sex Determination Analysis, X Chromosome, Adolescent, Chromosomal translocation, Biology, Y chromosome, Fluorescence, Translocation, Genetic, Nucleic acid thermodynamics, Y Chromosome, Genetics, medicine, Humans, Genetics (clinical), X chromosome, Sex Chromosome Aberrations, medicine.diagnostic_test, Cytogenetics, Nuclear Proteins, Nucleic Acid Hybridization, molecular cytogenetic analysis, Molecular biology, Sex-Determining Region Y Protein, DNA-Binding Proteins, Blotting, Southern, Testis determining factor, Molecular probe, DNA Probes, Fluorescence in situ hybridization, Transcription Factors
Abstract: XX maleness is the most common condition in which testes develop in the absence of a cytogenetically detectable Y chromosome. Using molecular techniques, it is possible to detect Yp sequences in the majority of XX males. In this study, we could detect Y-specific sequences, including the sex-determining region of the Y chromosome (SRY), using fluorescence in situ hybridization. In 5 out of 6 previously unpublished XX males, SRY was translocated onto the terminal part of an X chromosome. This is the first report in which translocation of an SRY-bearing fragment to an X chromosome in XX males could be directly demonstrated.
Published: 1992

31. Loss of constitutional heterozygosity in human astrocytomas

Author: E. Van de Keift, J. J. Martin, B. Van der Auwera, K. De Boulle, P. J. Willems, and P. Selosse
Subjects: Genetic Markers, Male, Heterozygote, Astrocytoma, law.invention, Loss of heterozygosity, Pathogenesis, law, Genotype, Medicine, Humans, Genes, Tumor Suppressor, Gene, Genetics, Chromosome Aberrations, business.industry, Brain Neoplasms, Chromosomes, Human, Pair 10, Brain, DNA, Neoplasm, medicine.disease, Blotting, Southern, Suppressor, Surgery, Female, Neurology (clinical), Restriction fragment length polymorphism, business, DNA Probes, Glioblastoma, Polymorphism, Restriction Fragment Length, Chromosomes, Human, Pair 17
Abstract: Inactivation of tumour suppressor genes or anti-oncogenes as well as activation of dominant acting oncogenes seem to be important mechanisms in the pathogenesis of gliomas. We compared constitutional and tumoural genotypes at different restriction fragment length polymorphism loci (RFLP) on chromosomes 10 and 17 in 15 unrelated individuals. Loss of heterozygosity (LOH) pointing to chromosomal loss or deletions was detected for at least one chromosome 17 marker in 11 gliomas (astrocytomas grades I-III and glioblastoma multiforme), whereas LOH for chromosome 10 loci was only detected in 3 out of 9 cases of glioblastoma multiforme and was not detected in low grade gliomas. Since LOH for chromosome 10 loci seems to be restricted only to glioblastoma multiforme, it is possible that recessive mutations on chromosome 10 are engaged in tumour progression from astrocytomas to glioblastoma multiforme. As LOH of chromosome 17 markers occurs in astrocytomas as in glioblastoma multiforme, chromosome 17 loci probably are involved in early tumour development.
Published: 1992

32. DNA diagnosis of cystic fibrosis by direct detection of the delta F508 mutation

Author: J, Hendrickx, J, Wauters, P, Coucke, L, Vits, B, Van der Auwera, and P J, Willems
Subjects: Cystic Fibrosis, Mutation, Humans, Electrophoresis, Polyacrylamide Gel, DNA, Polymerase Chain Reaction
Abstract: Cystic fibrosis (CF) is one of the most frequent recessive disorders among Caucasians. DNA analysis is performed by linkage analysis with DNA markers tightly linked to the CF gene. Cloning and sequencing of the cystic fibrosis gene, however, revealed that the major disease mutation is a phenylalanine deletion at amino acid position 508 of the mature protein (delta F508). These recent discoveries open great perspectives for the diagnosis of cystic fibrosis and for the detection of carriers in the normal population. In the present study we have used the polymerase chain reaction to detect the delta F508 mutation. This mutation was present on 80.3% of the CF chromosomes in the Belgian population. Twenty-three of 740 normal individuals (3.1%) were heterozygous carriers. Therefore, the frequency of heterozygous carriers in the Belgian population is estimated to be about 3.9% or 1 in every 26 individuals.
Published: 1991

33. Polymorphism at the TNFa microsatellite locus modulates the genetic risk for IDDM in subjects carrying the HLA DQA10501-DQB10201/DQA10301-DQB10302 high risk genotype

Author: P. De Knijf, F. Schuit, B. Van der Auwera, A. H. Zwinderman, Albert Naipal, P. Hanifi Moghaddam, R. F. Schipper, Marius J. Giphart, Bart O. Roep, and F. K. Gorus
Subjects: Genetics, Immunology, Genotype, Immunology and Allergy, Microsatellite, Locus (genetics), Tumor necrosis factor alpha, Human leukocyte antigen, Genetic risk, Biology
Published: 1997
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34. Autumn scientific meeting of the Flemish Society of Neurology-Psychiatry, Antwerp, 26th September 1987 on muscle diseases

Author: B. Van der Auwera, M. Bruyland, Juliaan Leroy, J. Bergmans, J. J. Martin, and A Van Elsen
Subjects: medicine.medical_specialty, Flemish, Neurology, business.industry, medicine, language, Surgery, Neurology (clinical), General Medicine, Psychiatry, business, language.human_language
Published: 1988
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35. Sex- and season-dependent differences in C-peptide levels at diagnosis of immune-mediated type 1 diabetes

Author: L. Van Gaal, Ilse Weets, J. De Schepper, P. Van Rooy, I. Verschraegen, Frans Gorus, I. Truyen, Daniel Pipeleers, B. Van der Auwera, Marie-Christine Lebrethon, Harry Dorchy, Medical Biochemistry, Pathologic Biochemistry and Physiology, and Pediatrics
Subjects: Adult, Male, Genotype, Adolescent, type 1 diabetes, diagnosis, Endocrinology, Diabetes and Metabolism, Endocrinopathy, Autoimmunity, Immunopathology, Disease, medicine.disease_cause, Autoantibody, Belgium, HLA-DQ Antigens, Diabetes mellitus, Autoimmune disease, Internal Medicine, medicine, Humans, Registries, Age of Onset, Child, Autoantibodies, Sex Characteristics, Type 1 diabetes, C-Peptide, business.industry, Infant, medicine.disease, Phenotype, HLA-System, Diabetes Mellitus, Type 1, age, Child, Preschool, Immunology, Female, Season, Age of onset, business, Sex characteristics
Abstract: The incidence of type 1 diabetes varies according to age, sex and season of diagnosis. We investigated whether these and other clinical, biological and anthropometric parameters were correlated with residual beta cell function in newly diagnosed patients, since it is possible that the nature of external and/or genetic disease accelerators may be (partly) reflected in the inaugural disease presentation.The correlates of random C-peptide levels sampled shortly after diagnosis (median [interquartile range]: 3 [0-14] days) were studied by multivariate analysis in 1,883 islet-antibody-positive diabetic patients aged40 years who were diagnosed between 1989 and 2000.Higher C-peptide levels (above percentile 50 of patients) were associated with older age at diagnosis, female sex, diagnosis in the high-incidence season (October to March), less-decreased BMI (expressed as a standard deviation score), lower insulin requirements after stabilisation, lower prevalence of ketonuria and a less-increased glycaemia at diagnosis (all p0.001). C-peptide levels were not correlated with calendar year at diagnosis, duration of symptoms prior to diagnosis, HLA-DQ2/DQ8 genotype or islet antibody status.Sex- and season-dependent differences in residual functional beta cell mass and/or insulin resistance have been identified at diagnosis of type 1 diabetes. They may reflect differences in disease-precipitating external or lifestyle factors and should be further investigated longitudinally in prediabetes to further identify putative aetiological factors, which may provide targets for prevention.

36. Insulitis in the pancreas of non-diabetic organ donors under age 25 years with multiple circulating autoantibodies against islet cell antigens.

Author: Smeets S, De Paep DL, Stangé G, Verhaeghen K, Van der Auwera B, Keymeulen B, Weets I, Ling Z, In't Veld P, and Gorus F
Subjects: Adolescent, Age Factors, Biomarkers blood, Case-Control Studies, Cell Proliferation, Child, Child, Preschool, Diabetes Mellitus, Type 1 blood, Diabetes Mellitus, Type 1 pathology, Donor Selection, Female, Humans, Infant, Insulin-Secreting Cells pathology, Male, Young Adult, Antigens immunology, Autoantibodies blood, CD8-Positive T-Lymphocytes immunology, Diabetes Mellitus, Type 1 immunology, Insulin-Secreting Cells immunology, Islets of Langerhans Transplantation, Tissue Donors
Abstract: Autoantibodies against islet cell antigens are routinely used to identify subjects at increased risk of symptomatic type 1 diabetes, but their relation to the intra-islet pathogenetic process that leads to positivity for these markers is poorly understood. We screened 556 non-diabetic organ donors (3 months to 24 years) for five different autoantibodies and found positivity in 27 subjects, 25 single- and two double autoantibody-positive donors. Histopathological screening of pancreatic tissue samples showed lesion characteristic for recent-onset type 1 diabetes in the two organ donors with a high-risk profile, due to their positivity for multiple autoantibodies and HLA-inferred risk. Inflammatory infiltrates (insulitis) were found in a small fraction of islets (<5%) and consisted predominantly of CD3+CD8+ T-cells. Islets with insulitis were found in close proximity to islets devoid of insulin-positivity; such pseudo-atrophic islets were present in multiple small foci scattered throughout the pancreatic tissue or were found to be distributed with a lobular pattern. Relative beta cell area in both single and multiple autoantibody-positive donors was comparable to that in autoantibody-negative controls. In conclusion, in organ donors under age 25 years, insulitis and pseudo-atrophic islets were restricted to multiple autoantibody-positive individuals allegedly at high risk of developing symptomatic type 1 diabetes, in line with reports in older age groups. These observations may give further insight into the early pathogenetic events that may culminate in clinically overt disease., (© 2021. The Author(s).)
Published: 2021
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37. Accelerated Progression to Type 1 Diabetes in the Presence of HLA-A24 and -B18 Is Restricted to Multiple Islet Autoantibody-Positive Individuals With Distinct HLA-DQ and Autoantibody Risk Profiles.

Author: Balke EM, Balti EV, Van der Auwera B, Weets I, Costa O, Demeester S, Abrams P, Casteels K, Coeckelberghs M, Tenoutasse S, Keymeulen B, Pipeleers DG, and Gorus FK
Subjects: Adolescent, Adult, Child, Child, Preschool, Diabetes Mellitus, Type 1 blood, Diabetes Mellitus, Type 1 genetics, Diabetes Mellitus, Type 1 immunology, Disease Progression, Female, Genetic Predisposition to Disease, Genotype, Humans, Infant, Infant, Newborn, Insulin Antibodies blood, Male, Registries, Risk Factors, Young Adult, Autoantibodies blood, Autoimmunity genetics, Diabetes Mellitus, Type 1 pathology, HLA-A24 Antigen genetics, HLA-B18 Antigen genetics, HLA-DQ Antigens genetics, Islets of Langerhans immunology
Abstract: Objective: We investigated the effect of HLA class I risk alleles on disease progression in various phases of subclinical islet autoimmunity in first-degree relatives of patients with type 1 diabetes., Research Design and Methods: A registry-based group of siblings/offspring (aged 0-39 years) was monitored from single- to multiple-autoantibody positivity ( n = 267) and from multiple-autoantibody positivity to clinical onset ( n = 252) according to HLA-DQ , -A*24 , -B*18 , and -B*39 status. Genetic markers were determined by PCR sequence-specific oligotyping., Results: Unlike HLA-B*18 or -B*39 , HLA-A*24 was associated with delayed progression from single- to multiple-autoantibody positivity ( P = 0.009) but not to type 1 diabetes. This occurred independently from older age ( P < 0.001) and absence of HLA-DQ2/DQ8 or -DQ8 (P < 0.001 and P = 0.003, respectively), and only in the presence of GAD autoantibodies. In contrast, HLA-A*24 was associated with accelerated progression from multiple-autoantibody positivity to clinical onset ( P = 0.006), but its effects were restricted to HLA-DQ8 + relatives with IA-2 or zinc transporter 8 autoantibodies ( P = 0.002). HLA-B*18, but not -B*39, was also associated with more rapid progression, but only in HLA-DQ2 carriers with double positivity for GAD and insulin autoantibodies ( P = 0.004)., Conclusions: HLA-A*24 predisposes to a delayed antigen spreading of humoral autoimmunity, whereas HLA-A*24 and -B*18 are associated with accelerated progression of advanced subclinical autoimmunity in distinct risk groups. The relation of these alleles to the underlying disease process requires further investigation. Their typing should be relevant for the preparation and interpretation of observational and interventional studies in asymptomatic type 1 diabetes., (© 2018 by the American Diabetes Association.)
Published: 2018
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38. Validation of an enzyme-linked immunosorbent assay for C-peptide analysis in Cameroon.

Author: Asanghanwa M, van Genderen F, Verhaeghen K, Van der Auwera B, Sobngwi E, Mbanya JC, and van Schravendijk C
Subjects: Cameroon, Cross Reactions, Enzyme-Linked Immunosorbent Assay, Female, Humans, Limit of Detection, Male, Materials Testing, Poverty Areas, Protein Stability, Reference Values, Reproducibility of Results, C-Peptide blood
Abstract: Aims: To validate an ELISA method for C-peptide analysis in Cameroon., Methods: We evaluated the linearity, detection limit, functional sensitivity, precision and accuracy, and further investigated for cross-reactivity by proinsulin, and interferences by lipids, bilirubin and hemoglobin. This method was compared with the Roche electrochemiluminescence immunoassay. C-peptide stability was assessed following a series of freeze-thaw cycles, and after storage at room temperature. The C-peptide reference range was determined by analyzing fifty plasma samples of Cameroonians without diabetes., Results: The ELISA was linear at least up to 7.09 μg/L, and had a detection limit of 0.09 μg/L, and a functional sensitivity of 0.32 μg/L. The inter- and intraassay %CV were 2.9-9.9%, and 5.2-9.4%, respectively. Recoveries were 81-94% in serum, and 93-98% in buffer. Comparison with the ECLIA yielded a good correlation coefficient (R(2)=0.98). There was no cross-reactivity with proinsulin, and no interference with lipids, bilirubin and hemoglobin. C-peptide was stable at room temperature for 24 h and up to 7 freeze-thaw cycles for medium (1-6 μg/L) and high (>6 μg/L) levels (<-15°C and <-70°C). The reference range for C-peptide was 0.38-3.63 μg/L., Conclusions: This method is suitable for C-peptide analysis in low-income countries like Cameroon., (Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.)
Published: 2012
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39. Graves hyperthyroidism after stopping immunosuppressive therapy in type 1 diabetic Islet cell recipients with pretransplant TPO autoantibodies.

Author: Gillard P, Huurman V, Van der Auwera B, Decallonne B, Poppe K, Roep BO, Gorus F, Mathieu C, Pipeleers D, and Keymeulen B
Subjects: Adult, Female, Humans, Male, Middle Aged, Autoantibodies immunology, Diabetes Mellitus, Type 1 therapy, Graves Disease diagnosis, Graves Disease etiology, Immunosuppressive Agents therapeutic use, Iodide Peroxidase immunology, Islets of Langerhans Transplantation adverse effects
Abstract: Objective: After an initially successful islet cell transplantation, a number of patients return to C-peptide negativity, and therefore immunosuppressive therapy is discontinued. Some are then found to have developed Graves disease. We examined the risk of Graves disease after immunosuppression., Research Design and Methods: Immunosuppressive therapy was stopped in 13 type 1 diabetic islet cell recipients who had received one course of antithymocyte globulin and maintenance doses of mycophenolate mofetil and a calcineurin inhibitor. None had a history of thyroid disease., Results: In four patients, clinical Graves hyperthyroidism was observed within 21 months after discontinuation and 30-71 months after the start of immunosuppressive therapy. All four patients exhibited a pretransplant positivity for thyroid peroxidase (TPO) autoantibodies, while the nine others were TPO negative pre- and posttransplantation., Conclusions: Type 1 diabetic recipients of islet cell grafts with pretransplant TPO autoantibody positivity exhibit a high risk for developing Graves hyperthyroidism after immunosuppressive therapy is discontinued for a failing graft.
Published: 2009
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40. Association of KIR2DL2 polymorphism rs2756923 with type 1 diabetes and preliminary evidence for lack of inhibition through HLA-C1 ligand binding.

Author: Ramos-Lopez E, Scholten F, Aminkeng F, Wild C, Kalhes H, Seidl C, Tonn T, Van der Auwera B, and Badenhoop K
Subjects: Alleles, Belgium, Cell Line, Tumor, Cytotoxicity, Immunologic genetics, Cytotoxicity, Immunologic immunology, Female, Genetic Predisposition to Disease, Genotype, Germany, HLA-C Antigens metabolism, Haplotypes genetics, Humans, Killer Cells, Natural immunology, Male, Polymorphism, Single Nucleotide genetics, Receptors, KIR2DL2 immunology, Diabetes Mellitus, Type 1 genetics, Gene Frequency genetics, HLA-C Antigens genetics, Killer Cells, Natural metabolism, Receptors, KIR2DL2 genetics
Abstract: Killer cell immunoglobulin-like receptors (KIRs) on chromosome 19q13.4 regulate the function of not only human natural killer (NK) cells but also T cells. An increase in activating KIR- human leucocyte antigen ligand pairs has been associated with an additional risk to develop type 1 diabetes (T1D). T1D families [n = 184 (552 individuals); n = 176 (528 subjects)], unrelated T1D patients (n = 380; n = 394) and healthy controls (n = 315; n = 401) from Germany and Belgium, respectively, were genotyped for the rs2756923 polymorphism within the KIR gene cluster haplotype B in exon 8 of the KIR2DL2 gene. We observed in both Germans and Belgians an overtransmission of the allele 'G' of the KIR2DL2-rs2756923 polymorphism (64.2% vs 35.8%, P = 3 x 10(-4) and 60.0% vs 40.0%, P = 0.02, respectively). In addition, this allele was more frequent in German patients than in healthy controls (78.4% vs 21.6%, P = 1 x 10(-3)). Preliminary results from a cytotoxicity assay suggest that inhibition of NK-cell cytotoxicity may be impaired in individuals carrying the rs2756923 G allele. These data suggest a potential role of the KIR2DL2-rs2756923 polymorphism in T1D in Germans and Belgians.
Published: 2009
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41. Screening for insulitis in adult autoantibody-positive organ donors.

Author: In't Veld P, Lievens D, De Grijse J, Ling Z, Van der Auwera B, Pipeleers-Marichal M, Gorus F, and Pipeleers D
Subjects: Adult, Biomarkers, Diabetes Mellitus, Type 1 epidemiology, Genetic Markers, Humans, Insulin Antibodies blood, Insulin Secretion, Insulin-Secreting Cells transplantation, Patient Selection, Tissue Banks, Autoantibodies blood, Diabetes Mellitus, Type 1 immunology, Insulin metabolism, Insulin-Secreting Cells immunology, Mass Screening, Pancreatic Diseases epidemiology, Tissue Donors statistics & numerical data
Abstract: Antibodies against islet cell antigens are used as predictive markers of type 1 diabetes, but it is unknown whether they reflect an ongoing autoimmune process in islet tissue. We investigated whether organs from adult donors that are positive for autoantibodies (aAbs) against islet cell antigens exhibit insulitis and/or a reduced beta-cell mass. Serum from 1,507 organ donors (age 25-60 years) was analyzed for islet cell antibodies (ICAs), glutamate decarboxylase aAbs (GADAs), insulinoma-associated protein 2 aAbs (IA-2As), and insulin aAbs. Tissue from the 62 aAb+ donors (4.1%) and from matched controls was examined for the presence of insulitis and for the relative area of insulin+ cells. Insulitis was detected in two cases; it was found in 3 and 9% of the islets and consisted of CD3+/CD8+ T-cells and CD68+ macrophages; in one case, it was associated with insulin+ cells that expressed the proliferation marker Ki67. Both subjects belonged to the subgroup of three donors with positivity for ICA, GADA, and IA-2-Ab and for the susceptible HLA-DQ genotype. Comparison of relative beta-cell area in aAb+ and aAb- donors did not show a significant difference. Insulitis was found in two of the three cases that presented at least three aAbs but in none of the other 59 antibody+ subjects or 62 matched controls. It was only detected in <10% of the islets, some of which presented signs of beta-cell proliferation. No decrease in beta-cell mass was detected in cases with insulitis or in the group of antibody+ subjects.
Published: 2007
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42. Sex- and season-dependent differences in C-peptide levels at diagnosis of immune-mediated type 1 diabetes.

Author: Weets I, Truyen I, Verschraegen I, Van der Auwera B, De Schepper J, Dorchy H, Lebrethon MC, Van Gaal L, Van Rooy P, Pipeleers DG, and Gorus FK
Subjects: Adolescent, Adult, Age of Onset, Autoantibodies blood, Belgium epidemiology, Child, Child, Preschool, Diabetes Mellitus, Type 1 diagnosis, Diabetes Mellitus, Type 1 epidemiology, Diabetes Mellitus, Type 1 immunology, Female, HLA-DQ Antigens blood, Humans, Infant, Male, Registries, Sex Characteristics, C-Peptide blood, Diabetes Mellitus, Type 1 blood
Abstract: Aims/hypothesis: The incidence of type 1 diabetes varies according to age, sex and season of diagnosis. We investigated whether these and other clinical, biological and anthropometric parameters were correlated with residual beta cell function in newly diagnosed patients, since it is possible that the nature of external and/or genetic disease accelerators may be (partly) reflected in the inaugural disease presentation., Materials and Methods: The correlates of random C-peptide levels sampled shortly after diagnosis (median [interquartile range]: 3 [0-14] days) were studied by multivariate analysis in 1,883 islet-antibody-positive diabetic patients aged <40 years who were diagnosed between 1989 and 2000., Results: Higher C-peptide levels (above percentile 50 of patients) were associated with older age at diagnosis, female sex, diagnosis in the high-incidence season (October to March), less-decreased BMI (expressed as a standard deviation score), lower insulin requirements after stabilisation, lower prevalence of ketonuria and a less-increased glycaemia at diagnosis (all p < 0.001). C-peptide levels were not correlated with calendar year at diagnosis, duration of symptoms prior to diagnosis, HLA-DQ2/DQ8 genotype or islet antibody status., Conclusions/interpretation: Sex- and season-dependent differences in residual functional beta cell mass and/or insulin resistance have been identified at diagnosis of type 1 diabetes. They may reflect differences in disease-precipitating external or lifestyle factors and should be further investigated longitudinally in prediabetes to further identify putative aetiological factors, which may provide targets for prevention.
Published: 2006
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43. Combined positivity for HLA DQ2/DQ8 and IA-2 antibodies defines population at high risk of developing type 1 diabetes.

Author: Decochez K, Truyen I, van der Auwera B, Weets I, Vandemeulebroucke E, de Leeuw IH, Keymeulen B, Mathieu C, Rottiers R, Pipeleers DG, and Gorus FK
Subjects: Adolescent, Adult, Child, Diabetes Mellitus, Type 1 blood, Diabetes Mellitus, Type 1 immunology, Disease Progression, Disease-Free Survival, Family, Family Health, Female, Genotype, Glutamate Decarboxylase immunology, Haplotypes genetics, Haplotypes immunology, Humans, Insulin Antibodies blood, Male, Prospective Studies, Regression Analysis, Risk Factors, Time Factors, Autoantibodies blood, Diabetes Mellitus, Type 1 genetics, HLA-DQ Antigens genetics
Abstract: Aims/hypothesis: Prevention trials in first-degree relatives of type 1 diabetic patients are hampered by large interindividual differences in progression rate to diabetes. We investigated whether specific combinations of immune and genetic markers can identify subgroups with more homogeneous progression to clinical onset., Methods: Antibodies against islet cell cytoplasm (ICA), insulin (IAA), glutamate decarboxylase (GADA) and IA-2 protein (IA-2A) were measured in 790 non-diabetic control subjects and 4,589 first-degree relatives under age 40., Results: On first sampling, 11.1% of the siblings presented at least one antibody type (p<0.001 vs other relatives). During follow-up (median 52 months) 43 subjects developed type 1 diabetes (31 siblings, ten offspring of a diabetic father, two offspring of a diabetic mother). Using Kaplan-Meier survival analysis and Cox regression, IA-2A conferred the highest 5-year diabetes risk (>50%) irrespective of the number of antibodies present. In initially IA-2A-positive relatives (n=58) progression to hyperglycaemia depended more on HLA DQ status than on type of kinship (84% progression in the presence of DQ2/DQ8 vs 32% in its absence; p<0.003). In IA-2A-negative relatives (n=4,531) 5-year progression to diabetes increased with the number of other antibodies (ICA, GADA and/or IAA) (p<0.001) but overall did not exceed 10% even for two or more antibodies. Among relatives initially positive for one or more antibody type other than IA-2A (n=315), there was significantly more progression to diabetes (overall still <10%) in carriers of DQ2 (p<0.001 vs no DQ2), regardless of DQ8 status., Conclusions/interpretation: These observations suggest that the HLA-DQ-inferred risk of diabetes can proceed through two distinct pathways distinguished by IA-2A status. Combined positivity for DQ2/DQ8 and IA-2A defines a more homogeneous high-risk population for prevention trials than those used so far.
Published: 2005
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44. Relation between disease phenotype and HLA-DQ genotype in diabetic patients diagnosed in early adulthood.

Author: Weets I, Siraux V, Daubresse JC, De Leeuw IH, Féry F, Keymeulen B, Krzentowski G, Letiexhe M, Mathieu C, Nobels F, Rottiers R, Scheen A, Van Gaal L, Schuit FC, Van der Auwera B, Rui M, De Pauw P, Kaufman L, and Gorus FK
Subjects: Adolescent, Adult, Autoantibodies analysis, Diabetes Mellitus physiopathology, Female, Genotype, Humans, Male, Phenotype, Diabetes Mellitus genetics, Diabetes Mellitus immunology, HLA-DQ Antigens genetics
Abstract: We investigated inaugural disease phenotype in relation to the presence or absence of diabetes-associated autoantibodies and human leukocyte antigen (HLA) DQ risk genotypes in adult-onset diabetic patients. Blood samples and questionnaires were obtained from 1584 recent-onset Belgian Caucasian patients (age 15-39 yr at diagnosis of primary diabetes) who were recruited by the Belgian Diabetes Registry over an 11-yr period. At clinical diagnosis, antibody-positive patients (n = 1198) were on average younger and had more symptoms, a more acute disease onset, lower body mass index, and random C-peptide levels, but higher insulin needs, glycemia, and prevalence of ketonuria, HLA-DQ, and 5' insulin gene susceptibility genotypes (P < 0.001 vs. antibody-negative patients; n = 386). In antibody-positive patients, these characteristics did not differ according to HLA-DQ genotype. However, in antibody-negative subjects, we found that patients were younger (P = 0.001); had a lower body mass index (P < 0.001), higher insulin needs (P = 0.014), and amylasemia (P = 0.001); and tended to have a higher glycemia and lower C-peptide in the presence of susceptible HLA-DQ genotypes. Differences according to HLA-DQ genotype subsisted after careful age-matching. In conclusion, we found no relation between initial disease phenotype and HLA-DQ genotype in antibody-positive diabetic young adults. In contrast, antibody-negative patients displayed more type 1-like features when carrying susceptible HLA-DQ genotypes known to promote the development of antibody-positive diabetes. The overrepresentation of these susceptibility genotypes in antibody-negative patients suggests the existence of an immune-mediated disease process with as yet unidentified immune markers in a subgroup of seronegative patients.
Published: 2002
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45. Genetic structure of IDDM1: two separate regions in the major histocompatibility complex contribute to susceptibility or protection. Belgian Diabetes Registry.

Author: Hanifi Moghaddam P, de Knijf P, Roep BO, Van der Auwera B, Naipal A, Gorus F, Schuit F, and Giphart MJ
Subjects: Adult, Alleles, Female, Gene Frequency, Genetic Markers, Genotype, HLA-DQ Antigens genetics, HLA-DQ alpha-Chains, HLA-DQ beta-Chains, Haplotypes, Humans, Linkage Disequilibrium, Male, Microsatellite Repeats, Polymerase Chain Reaction, Tumor Necrosis Factor-alpha genetics, Diabetes Mellitus, Type 1 genetics, Major Histocompatibility Complex
Abstract: We analyzed 11 markers in the IDDM1 region in 120 IDDM patients and 83 healthy control subjects who were fully matched for the highest risk HLA-DQA1*0301-DQB1 *0302/DQA1*0501-DQB1*0201 genotype. Our study provides strong evidence that two regions in the major histocompatibility complex contribute to IDDM susceptibility or protection. First, despite selection for highest IDDM-associated risk DQ genotypes, this region displays extensive linkage disequilibrium (LD) differences between IDDM patients and control subjects. A second critical region was mapped around the microsatellite locus D6S273 centromeric of TNF, and it is approximately 200 kb in size. LD analysis shows that "diabetogenic haplotypes" may have resulted from a recombination telomeric of D6S1014 in the region of D6S273 and TNFa. Haplotype analysis using HLA and microsatellite loci refines IDDM risk assessment in carriers of the HLA-DQ highest risk genotype.
Published: 1998

46. Increased prevalence of abnormal immunoglobulin M, G, and A concentrations at clinical onset of insulin-dependent diabetes mellitus: a registry-based study. The Belgian Diabetes Registry.

Author: Gorus FK, Vandewalle CL, Winnock F, Lebleu F, Keymeulen B, Van der Auwera B, Falorni A, Dorchy H, Féry F, and Pipeleers DG
Subjects: Adolescent, Adult, Aging, Biomarkers, Child, Child, Preschool, Diabetes Mellitus, Type 1 genetics, Female, Fructosamine blood, HLA-DQ Antigens genetics, Humans, Infant, Insulin administration & dosage, Insulin genetics, Lipase blood, Male, Multivariate Analysis, Polymorphism, Restriction Fragment Length, Reference Values, Sex Characteristics, Diabetes Mellitus, Type 1 immunology, Immunoglobulin A blood, Immunoglobulin G blood, Immunoglobulin M blood, Registries
Abstract: In view of the reported association of insulin-dependent diabetes mellitus (IDDM) with viral infections, (non-) islet-specific immune changes, and partial immunodeficiencies, we used immunonephelometry to measure circulating levels of IgM, IgG, and IgA in a registry-based group of IDDM patients under age 40 years at clinical onset (n = 397) and in age-matched nondiabetic siblings (n = 316) and control subjects (n = 322). Overall, IgM and IgA concentrations were higher, and IgG concentrations lower, in patients than in control subjects or siblings (P < 0.001). In siblings, IgM concentrations were higher than in control subjects (P < 0.001). Using age-adjusted reference intervals, abnormal Ig concentrations were noted in 27% of the patients at onset versus only 10% of the siblings and 7% of the control subjects (P < 0.001). For onset between 20 and 40 years (n = 220), 30% of the patients presented either increased IgM levels (21%) or decreased IgG levels (11%). Both independent phenomena occurred regardless of diabetes-associated immune and genetic markers. In patients and siblings, IgM levels were positively correlated with pancreatic lipase activity. In diabetic children (0-9 years; n = 65), a subgroup presented increased IgA levels (15%) in association with the highest HLA DQ-linked genetic risk and elevated IgM levels. The changes in total Ig concentrations at onset were largely reversed under insulin therapy. They may reflect exposure to environmental triggers, such as viral infections, or to (relative) insulinopenia prior to clinical disease onset. Whatever their cause, different serum Ig levels exist in different age groups of recent-onset IDDM patients.
Published: 1998
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47. Associations of GAD65- and IA-2- autoantibodies with genetic risk markers in new-onset IDDM patients and their siblings. The Belgian Diabetes Registry.

Author: Vandewalle CL, Falorni A, Lernmark A, Goubert P, Dorchy H, Coucke W, Semakula C, Van der Auwera B, Kaufman L, Schuit FC, Pipeleers DG, and Gorus FK
Subjects: Adolescent, Adult, Belgium, Child, Child, Preschool, Diabetes Mellitus, Type 1 blood, Female, Genetic Markers, Genotype, Humans, Infant, Insulin genetics, Male, Registries, Risk Factors, Autoantibodies blood, Diabetes Mellitus, Type 1 genetics, Diabetes Mellitus, Type 1 immunology, Glutamate Dehydrogenase immunology, HLA-DQ Antigens genetics, Nuclear Family
Abstract: Objective: To investigate the association of GAD (65-kDa) autoantibodies (GAD65-Abs) and IA-2 autoantibodies (IA-2-Abs) with human leukocyte antigen (HLA)-DQ and insulin gene (INS) risk markers in patients with recent-onset IDDM and their siblings., Research Design and Methods: Blood was sampled from 608 recent-onset IDDM patients and 480 siblings, aged 0-39 years and consecutively recruited by the Belgian Diabetes Registry, to determine GAD65- and IA-2-Ab (radiobinding assay), HLA-DQ- (allele-specific oligonucleotyping), and INS-genotypes (restriction fragment length polymorphism analysis; siblings, n = 439)., Results: At the onset of IDDM, GAD65-Abs were preferentially associated with two populations at genetic risk but only in the 20- to 39-year age-group: 1) their prevalence was higher in carriers of DQA1*0301-DQB1*0302 (88 vs. 73% in non[DQA1*0301-DQB1*0302], P = 0.001), and 2) an association was found in patients lacking this haplotype but carrying DQA1*0501-DQB1*0201, together with INS I/I (87 vs. 54% vs. non[INS I/I], P = 0.003). Siblings of IDDM patients also presented the association of GAD65-Abs with DQA1*0301-DQB1*0302 (13 vs. 2% non[DQA1*0301-DQB1*0302], P < 0.001), while associations with the second genetic risk group could not yet be assessed. At the onset of IDDM, IA-2-Ab prevalence was higher in carriers of DQA1*0301-DQB1*0302 (69 vs. 39% non[DQA1*0301-DQB1*0302], P < 0.001) but not of DQA1*0501-DQB1*0201 or INS I/I. This association was present in both the 0- to 19- and the 20- to 39-year age-groups. It was also found in siblings of IDDM patients (4 vs. 0% non[DQA1*0301-DQB1*0302], P < 0.001)., Conclusions: Both GAD65- and IA-2-Abs exhibit higher prevalences in presence of HLA-DQ- and/or INS-genetic risk markers. Their respective associations differ with age at clinical onset, suggesting a possible usefulness in the identification of subgroups in this heterogeneous disease.
Published: 1997
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48. TNFa microsatellite polymorphism modulates the risk of IDDM in Caucasians with the high-risk genotype HLA DQA10501-DQB10201/DQA10301-DQB10302. Belgian Diabetes Registry.

Author: Moghaddam PH, Zwinderman AH, de Knijff P, Roep BO, Schipper RF, Van der Auwera B, Naipal A, Gorus F, Schuit F, and Giphart MJ
Subjects: Epistasis, Genetic, HLA-DQ alpha-Chains, HLA-DQ beta-Chains, Haplotypes, Humans, Microsatellite Repeats, Polymorphism, Genetic, Risk Factors, Diabetes Mellitus, Type 1 genetics, HLA-DQ Antigens genetics, Tumor Necrosis Factor-alpha genetics
Published: 1997
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49. Genetic susceptibility for insulin-dependent diabetes mellitus in Caucasians revisited: the importance of diabetes registries in disclosing interactions between HLA-DQ- and insulin gene-linked risk. Belgian Diabetes Registry.

Author: van der Auwera B, Schuit F, Lyaruu I, Falorni A, Svanholm S, Vandewalle CL, and Gorus FK
Subjects: Adolescent, Adult, Age of Onset, Child, Child, Preschool, Female, Genes, Genetic Predisposition to Disease, Genotype, Humans, Infant, Infant, Newborn, Male, Middle Aged, Polymorphism, Genetic, Risk, Diabetes Mellitus, Type 1 genetics, HLA-DQ Antigens genetics, Insulin genetics, Registries, White People genetics
Abstract: Whether genetic susceptibility for insulin-dependent diabetes mellitus (IDDM) at the 5' insulin gene polymorphic region (5' INS) interacts with human leukocyte antigen (HLA)-DQ-linked disease risk and whether it is associated with autoantibody formation is presently controversial. Diabetes registries allow more systematic reassessment of these questions. Two hundred and ninety-six Caucasian IDDM patients were recruited by the Belgian Diabetes Registry and sampled at disease onset, together with 195 ethnically matched control subjects. 5'INS genotypes were determined by Southern blotting, HLA-DQ by allele-specific oligotyping, and autoantibodies by validated immunoassays. The 5' INS 1/1 genotype was more prevalent in patients than in controls [relative risk (RR) = 2.3; P < 10(-4)]. Regardless of age at onset, the 5' INS 1/1 genotype occurred less frequently in patients with the high-risk genotype DQA1*0301-DQB1*0302/DQA1*0501-DQB1*0201 than in patients without it (P < 0.04). The RR associated with this high-risk HLA-DQ genotype (24.9; P < 10(-6)) was not affected by the presence or absence of the 5' INS 1/1 genotype. Combined positivity for the 5' INS 1/1 genotype and for one of three other HLA-DQ genotypes associated with an intermediate risk for IDDM conferred an age-independent RR of 12.1 (P < 10(-4)). In the absence of the 5' INS 1/1 genotype, intermediate-risk HLA-DQ genotypes no longer conferred a significant risk (2.9; not significantly different from 1). In subjects carrying neutral, protective, or infrequent HLA-DQ genotypes, the overall RR for IDDM was significantly lower than 1 (0.2; P < 10(-6)) in the absence of the 5' INS 1/1 genotype but not in its presence (0.8; not significantly different from 1). The 5' INS 1/1 genotype was not preferentially associated with immune markers for IDDM. In conclusion, regardless of age at onset and the presence of autoantibodies, 5' INS polymorphisms contribute preferentially to IDDM susceptibility in subjects without the highest HLA-DQ-associated risk.
Published: 1995
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50. DRB10403 protects against IDDM in Caucasians with the high-risk heterozygous DQA10301-DQB10302/DQA10501-DQB1*0201 genotype. Belgian Diabetes Registry.

Author: Van der Auwera B, Van Waeyenberge C, Schuit F, Heimberg H, Vandewalle C, Gorus F, and Flament J
Subjects: Alleles, Base Sequence, DNA Probes genetics, Diabetes Mellitus, Type 1 prevention & control, Female, Gene Frequency, Genetic Markers, Genotype, HLA-DQ Antigens genetics, HLA-DQ alpha-Chains, HLA-DQ beta-Chains, HLA-DRB1 Chains, Haplotypes, Heterozygote, Humans, Male, Molecular Sequence Data, Risk Factors, White People genetics, Diabetes Mellitus, Type 1 genetics, Diabetes Mellitus, Type 1 immunology, HLA-DR Antigens genetics
Abstract: The human leukocyte antigen (HLA) class II genotype DQA1*0301-DQB1*0302/DQA1*0501-DQB1*0201 has been identified as a marker strongly predisposing to insulin-dependent diabetes mellitus (IDDM) in Caucasian populations. Its frequency in control populations (1-3%) is still, however, 1 order of magnitude higher than the prevalence of IDDM, suggesting that its penetrance can be modified by protective factors. In this study we searched for such a factor in the DRB1 locus by studying DRB1*04 polymorphism in 174 European Caucasian IDDM patients and 73 nondiabetic control subjects, all sharing the HLA-DR3/DR4 phenotype. Significant protection was encoded by the DRB1*0403 allele, which was observed in 5 of 49 control subjects (10%) and none of 171 IDDM patients (0%) with the DQA1*0301-DQB1*0302/DQA1*0501-DQB1*0201 genotype (RR = 0.02 [0.01-0.18], P < 0.0005). These data support the concept that protective HLA class II genes can overrule the risk caused by HLA-DQ susceptibility dimers. They also contribute to a possible strategy to screen for nondiabetic individuals with increased genetic risk of developing IDDM.
Published: 1995
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