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4 results on '"Annette Knopff"'

1. Landmark models to define the age-adjusted risk of developing stage 1 type 1 diabetes across childhood and adolescence

Author

Verena Sophia Hoffmann, Andreas Weiß, Christiane Winkler, Annette Knopff, Manja Jolink, Ezio Bonifacio, and Anette-G. Ziegler

Subjects
Autoimmunity, Islet autoantibodies, Type 1 diabetes, Landmark risk, Medicine
Abstract

Abstract Background Autoimmune diseases are often preceded by an asymptomatic autoantibody-positive phase. In type 1 diabetes, the detection of autoantibodies to pancreatic islet antigens in genetically at-risk children is prognostic for future clinical diabetes. Testing for islet autoantibodies is, therefore, performed in a range of clinical studies. Accurate risk estimates that consider the a priori genetic risk and other risk modifiers are an important component of screening. The age of an individual is an under-appreciated risk modifier. The aim of this study was to provide age-adjusted risk estimates for the development of autoantibodies across childhood in genetically at-risk children. Methods The prospective BABYDIAB and BABYDIET studies included 2441 children from birth who had a first-degree relative with type 1 diabetes. Children were born between 1989 and 2006 and were regularly followed from birth for the development of islet autoantibodies and diabetes. A landmark analysis was performed to estimate the risk of islet autoantibodies at birth and at the age 3.5, 6.5 and 12.5 years. Exponential decay curves were fitted for the risk by the age of 20 years. Results The risk of islet autoantibodies by the age of 20 years was 8%, 4.6%, 2.6% and 0.9%, at the landmark ages of birth, 3.5, 6.5 and 12.5 years, respectively. The short-term risks (within 6 years of follow-up) at these landmark ages were 5.3%, 2.9%, 1.8% and 1%, respectively. The decline in autoantibody risk with age was modelled using a one-phase exponential decay curve (r = 0.99) with a risk half-life of 3.7 years. This risk decay model was remarkably consistent when the outcome was defined as islet autoantibody-positive or multiple islet autoantibody-positive and when the study cohort was stratified by HLA risk genotype. A similar decay model was observed for coeliac disease-associated transglutaminase antibodies in the same cohort. Unlike the risk of developing islet autoantibodies, the rate of developing clinical diabetes in children who were islet autoantibody-positive did not decline with age. Conclusion The risk of developing autoantibodies drops exponentially with age in children with a first-degree relative with type 1 diabetes.

Published
2019
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2. Type 1 diabetes vaccine candidates promote human Foxp3+Treg induction in humanized mice

Author

Isabelle Serr, Rainer W. Fürst, Peter Achenbach, Martin G. Scherm, Füsun Gökmen, Florian Haupt, Eva-Maria Sedlmeier, Annette Knopff, Leonard Shultz, Richard A. Willis, Anette-Gabriele Ziegler, and Carolin Daniel

Subjects
Science
Abstract

Type 1 diabetes is associated with the loss of self-tolerance to the insulin-producing β-cells in the pancreas. Here the authors show that vaccination with insulin mimetopes can induce human insulin-specific regulatory T cells to mediate tolerance in a humanized mouse model.

Published
2016
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3. Effects of Gluten Intake on Risk of Celiac Disease: A Case-Control Study on a Swedish Birth Cohort

Author

Carin Andrén Aronsson, Hye-Seung Lee, Sibylle Koletzko, Ulla Uusitalo, Jimin Yang, Suvi M. Virtanen, Edwin Liu, Åke Lernmark, Jill M. Norris, Daniel Agardh, Marian Rewers, Kimberly Bautista, Judith Baxter, Ruth Bedoy, Daniel Felipe-Morales, Brigitte I. Frohnert, Patricia Gesualdo, Michelle Hoffman, Rachel Karban, Jill Norris, Adela Samper-Imaz, Andrea Steck, Kathleen Waugh, Hali Wright, Jin-Xiong She, Desmond Schatz, Diane Hopkins, Leigh Steed, Jamie Thomas, Janey Adams, Katherine Silvis, Michael Haller, Melissa Gardiner, Richard McIndoe, Ashok Sharma, Joshua Williams, Gabriela Foghis, Stephen W. Anderson, Richard Robinson, Anette G. Ziegler, Andreas Beyerlein, Ezio Bonifacio, Michael Hummel, Sandra Hummel, Kristina Foterek, Mathilde Kersting, Annette Knopff, Claudia Peplow, Roswith Roth, Joanna Stock, Elisabeth Strauss, Katharina Warncke, Christiane Winkler, Jorma Toppari, Olli G. Simell, Annika Adamsson, Heikki Hyöty, Jorma Ilonen, Sanna Jokipuu, Tiina Kallio, Miia Kähönen, Mikael Knip, Annika Koivu, Mirva Koreasalo, Kalle Kurppa, Maria Lönnrot, Elina Mäntymäki, Katja Multasuo, Juha Mykkänen, Tiina Niininen, Mia Nyblom, Petra Rajala, Jenna Rautanen, Anne Riikonen, Minna Romo, Satu Simell, Tuula Simell, Ville Simell, Maija Sjöberg, Aino Stenius, Maria Särmä, Sini Vainionpää, Eeva Varjonen, Riitta Veijola, Mari Vähä-Mäkilä, Mari Åkerlund, Maria Ask, Jenny Bremer, Ulla-Marie Carlsson, Corrado Cilio, Emelie Ericson-Hallström, Lina Fransson, Thomas Gard, Joanna Gerardsson, Rasmus Bennet, Monica Hansen, Gertie Hansson, Cecilia Harmby, Susanne Hyberg, Fredrik Johansen, Berglind Jonasdottir, Helena Elding Larsson, Sigrid Lenrick Forss, Markus Lundgren, Maria Månsson-Martinez, Maria Markan, Jessica Melin, Zeliha Mestan, Kobra Rahmati, Anita Ramelius, Anna Rosenquist, Falastin Salami, Sara Sibthorpe, Birgitta Sjöberg, Ulrica Swartling, Evelyn Tekum Amboh, Erika Trulsson, Carina Törn, Anne Wallin, Åsa Wimar, Sofie Åberg, William A. Hagopian, Michael Killian, Claire Cowen Crouch, Jennifer Skidmore, Stephen Ayres, Kayleen Dunson, Rachel Hervey, Corbin Johnson, Rachel Lyons, Arlene Meyer, Denise Mulenga, Elizabeth Scott, Joshua Stabbert, Alexander Tarr, Morgan Uland, John Willis, Dorothy Becker, Margaret Franciscus, MaryEllen Dalmagro-Elias Smith, Ashi Daftary, Mary Beth Klein, Chrystal Yates, Jeffrey P. Krischer, Michael Abbondondolo, Sarah Austin-Gonzalez, Sandra Baethke, Rasheedah Brown, Brant Burkhardt, Martha Butterworth, Joanna Clasen, David Cuthbertson, Christopher Eberhard, Steven Fiske, Dena Garcia, Jennifer Garmeson, Veena Gowda, Kathleen Heyman, Francisco Perez Laras, Shu Liu, Xiang Liu, Kristian Lynch, Jamie Malloy, Cristina McCarthy, Wendy McLeod, Steven Meulemans, Chris Shaffer, Laura Smith, Susan Smith, Noah Sulman, Roy Tamura, Kendra Vehik, Ponni Vijayakandipan, Keith Wood, Lori Ballard, David Hadley, Beena Akolkar, Kasia Bourcier, Thomas Briese, Suzanne Bennett Johnson, and Eric Triplett

Subjects
Male, medicine.medical_specialty, Glutens, Biopsy, Teddy Study, Diet, Pediatric, Wheat, The Environmental Determinants of Diabetes in the Young, Breastfeeding, Gastroenterology and Hepatology, digestive system, Gastroenterology, Risk Assessment, 03 medical and health sciences, 0302 clinical medicine, GTP-Binding Proteins, Internal medicine, Medicine, Humans, Protein Glutamine gamma Glutamyltransferase 2, 030212 general & internal medicine, Seroconversion, Child, Autoantibodies, 2. Zero hunger, chemistry.chemical_classification, Sweden, Transglutaminases, Hepatology, business.industry, Case-control study, nutritional and metabolic diseases, Infant, Odds ratio, ta3123, Gluten, digestive system diseases, Confidence interval, 3. Good health, Intestines, Celiac Disease, chemistry, Case-Control Studies, Child, Preschool, Immunology, 030211 gastroenterology & hepatology, Female, business, Risk assessment
Abstract

BACKGROUND & AIMS: It is not clear how intake of gluten during infancy affects subsequent risk of celiac disease. We investigated whether gluten intake before 2 years of age increases risk for celiac disease in genetically susceptible children. METHODS: We performed a case-control study of 436 pairs of children, generated from a database of 2525 children with genetic susceptibility to celiac disease in Sweden, matched for sex, birth year, and HLA genotype from September 2004 and February 2010. Children were screened annually for celiac disease using an assay for tissue transglutaminase autoantibodies (tTGA). Intestinal biopsies were collected from children who tested positive for tTGA to confirm the presence of celiac disease. Gluten intake was calculated from 3-day food records collected when the children were 9, 12, 18 and 24 months old. RESULTS: Breastfeeding duration (median 32 weeks) and age at first introduction to gluten (median 22 weeks) did not differ between cases and tTGA-negative children (controls). At the visit prior to tTGA seroconversion, cases reported a larger intake of gluten (median 4.9 g/day) than controls (median 3.9 g/day) (odds ratio [OR], 1.28; 95% confidence interval [CI], 1.13-1.46; P=.0002). More cases consumed amounts of gluten in the upper 3rd tertile (i.e. >5.0 g/day) before they tested positive for tTGA seroconversion than controls (OR, 2.65; 95% CI, 1.70-4.13; P

Published
2015

4. Mature high-affinity immune responses to (pro)insulin anticipate the autoimmune cascade that leads to type 1 diabetes

Author

Peter Achenbach, Kerstin Koczwara, Annette Knopff, Heike Naserke, Anette-G. Ziegler, and Ezio Bonifacio

Subjects
Insulin Antibodies, food and beverages, Infant, General Medicine, Binding, Competitive, Article, Cohort Studies, Epitopes, Islets of Langerhans, Diabetes Mellitus, Type 1, Haplotypes, Risk Factors, Child, Preschool, HLA-DR4 Antigen, Humans, Insulin, heterocyclic compounds, Amino Acid Sequence, Prospective Studies, Child, Autoantibodies, Proinsulin
Abstract

Children at risk for type 1 diabetes can develop early insulin autoantibodies (IAAs). Many, but not all, of these children subsequently develop multiple islet autoantibodies and diabetes. To determine whether disease progression is reflected by autoantibody maturity, IAA affinity was measured by competitive radiobinding assay in first and subsequent IAA-positive samples from children followed from birth in the BABYDIAB cohort. IAA affinity in first positive samples ranged from less than 10(6) l/mol to more than 10(11) l/mol. High affinity was associated with HLA DRB1*04, young age of IAA appearance, and subsequent progression to multiple islet autoantibodies or type 1 diabetes. IAA affinity in multiple antibody-positive children was on average 100-fold higher than in children who remained single IAA positive or became autoantibody negative. All high-affinity IAAs required conservation of human insulin A chain residues 8-13 and were reactive with proinsulin. In contrast, most lower-affinity IAAs were dependent on COOH-terminal B chain residues and did not bind proinsulin. These data are consistent with the concept that type 1 diabetes is associated with sustained early exposure to (pro)insulin in the context of HLA DR4 and show that high-affinity proinsulin-reactive IAAs identify children with the highest diabetes risk.

Published
2004
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