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21. Introduction

Author

Lefvert, A. K. and Hansson, G. K.

Published
2000

25. CTLA4 is expressed on mature dendritic cells derived from human monocytes and influences their maturation and antigen presentation

Author

Ni Zhen H, Vollenhoven Annika V, Anton Doina, Fan Zhong Z, Wang Xiong B, Chen Xiao F, and Lefvert Ann K

Subjects
Immunologic diseases. Allergy, RC581-607
Abstract

Abstract Background Dendritic cells (DCs) initiate immune responses through their direct interaction with effector cells. However, the mechanism by which DC activity is regulated is not well defined. Previous studies have shown that CTLA4 on T cells regulates DCs function by "cross-talk". We investigated whether there is an intrinsic regulatory mechanism in DCs, with CTLA4 as a candidate regulator. Results We confirmed via RT-PCR and flow cytometry the natural expression of CTLA4 on mature DCs derived from human monocytes. Approximately 8% CD1a-positive cells express CTLA4 both on surface and intracellular, whereas 10% CD1a-negative cells express CTLA4 intracellularly, but little expression was observed on the cell surface. The cross-linking of CTLA4 inhibits DCs maturation and antigen presentation in vitro, but does not inhibit endocytosis. Conclusions CTLA4 is expressed by DCs and plays an inhibitory role. CTLA4-expressing DCs may represent a group of regulatory DCs. Because of its wide distribution on different cell types, CTLA4 may play a general role in regulating immune responses.

Published
2011
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42. Mab 17-1A Used for Therapy of Patients with Metastatic Colorectal Carcinomas

Author

Mellstedt, H., Frödin, J.-E., Masucci, G., Lindemalm, C., Wedelin, C., Christensson, B., Shetye, J., Biberfeld, P., Lefvert, A.-K., Pihlstedt, P., Makower, J., Harmenberg, U., Wahren, B., Ahlman, B., Cedermark, B., Erwald, R., Magnusson, I., Nathansson, J., Rieger, A., Beger, Hans G., editor, Büchler, Markus, editor, Reisfeld, Ralph A., editor, and Schulz, Gregor, editor

Published
1989
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46. Overexpression of select T cell receptor V beta gene families within CD4+ and CD8+ T cell subsets of myasthenia gravis patients: a role for superantigen(s)?

Author

Gigliotti, D, Lefvert, A. K., Jeddi Tehrani, M, Esin, Semih, Hodara, V, Pirskanen, R, Wigzell, H, and Andersson, R.

Subjects
Adult, CD4-Positive T-Lymphocytes, Blotting, Southern, Superantigens, Myasthenia Gravis, Receptors, Antigen, T-Cell, Humans, CD8-Positive T-Lymphocytes, Middle Aged, Polymerase Chain Reaction, Aged, Research Article
Abstract

BACKGROUND: The principal symptoms of myasthenia gravis (MG), muscle weakness and fatigue due to impaired neuromuscular transmission, are caused by autoantibodies to the muscle nicotinic acetylcholine receptor (AChR). The mechanisms underlying the autoimmune response, however, appear to be initiated by activation of specific HLA class II-restricted CD4+ T lymphocytes. Thus, central to elucidating the causation of MG is determining how T cells are recruited to contribute to misguided immunological assaults on the major autoantigenic target, AChR. MATERIALS AND METHODS: By combining a polymerase chain reaction (PCR)-based strategy and Southern blot technique, we have analyzed the frequency of expression of 22 individual T cell receptor (TCR) V beta gene subfamilies in CD4+ and CD8+ peripheral blood T cell subsets derived from eight MG patients and seven healthy controls. The quantification of relative usage of individual TCR J beta gene segments was performed by hybridization of PCR-amplified products (specifically V beta 1-C beta) with a complete panel of 32P-5'-end-labeled J beta-specific oligonucleotide probes, followed by scanning analysis of autoradiographs. RESULTS: Comparisons of data obtained from V beta analyses of T cells from MG patients with those from healthy individuals established that MG patients significantly overexpressed V beta 1, V beta 13.2, V beta 17, and V beta 20 gene family members within both CD4+ and CD8+ T cell subpopulations. Moreover, analysis of the relative utilization of individual TCR J beta gene segments in V beta 1+/CD4+ and V beta 1+/CD8+ T lymphocytes revealed distribution patterns in patients indistinguishable from those recorded in the corresponding cell subsets derived from controls. CONCLUSIONS: T lymphocytes from MG patients displayed a biased overexpression of four TCR V beta gene segments: V beta 1, V beta 13.2, V beta 17, and V beta 20. The relative frequencies of association of individual V beta 1 (D beta) J beta combinations revealed that J beta gene usage in the V beta 1-over-represented T cell subsets had normal distribution patterns. It can thus be deduced that J beta gene segment products appear not to have a selective effect on the process leading to overexpression of V beta 1 exons in MG patients. Hence, our observations suggest a possible role for superantigen(s) in the T cell activation in MG patients.

Published
1996

47. beta2 Adrenoceptor gene single nucleotide polymorphisms are associated with rheumatoid arthritis in northern Sweden.

Author

Xu, B-Y, Arlehag, L, Rantapää-Dahlqvist, Solbritt, Lefvert, A K, Xu, B-Y, Arlehag, L, Rantapää-Dahlqvist, Solbritt, and Lefvert, A K

Abstract

Background: β2 Adrenoceptor (β2-AR) represents a link between the sympathetic nervous system and the immune system, and may be involved in human rheumatoid arthritis (RA). The gene encoding β2-AR contains three single nucleotide polymorphisms (SNPs) at amino acid positions 16, 27, and 164. Objective: To examine the common variants at positions 16 and 27 and their association with RA. Methods: An allele-specific polymerase chain reaction to determine the common variants at positions 16 and 27 was used in 154 patients with RA and 198 ethnically matched healthy subjects from northern Sweden. Results: Carriage of Arg16 and of Gln27 was associated with RA. Carriage of Gln27 was associated with activity of the disease and in combination with non-carriage of Arg16 with higher levels of rheumatoid factor. Conclusion: The β2-AR SNPs may thus constitute an additional non-major histocompatibility complex association in RA.

Published
2005
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48. Beta2-adrenergic receptor gene single-nucleotide polymorphisms are associated with rheumatoid arthritis in northern Sweden.

Author

Xu, B, Arlehag, L, Rantapää-Dahlqvist, Solbritt, Lefvert, A K, Xu, B, Arlehag, L, Rantapää-Dahlqvist, Solbritt, and Lefvert, A K

Abstract

The beta2-adrenergic receptor (beta2-AR) belongs to the group of G-protein-coupled receptors and is present on skeletal and cardiac muscle cells and on lymphocytes. The gene encoding beta2-AR (ADRB2) displays a moderate degree of heterogeneity in the human population and the distributions of single-nucleotide polymorphisms (SNPs) at amino acid positions 16, 27, and 164 are changed in asthma, obesity, and hypertension and in the autoimmune disease myasthenia gravis. An involvement of the beta2-AR has also been suggested in human rheumatoid arthritis (RA) and its animal model. We describe here an increased prevalence of the alleles Arg16 and Gln27 and a lower prevalence of homozygosis for Gly16 and Glu27 in patients with RA. Patients having the genotype combination GlyGly16-GlnGlu27 had higher levels of rheumatoid factor (RF) and a more active disease than other patients. Patients having the genotype Arg16-Gln27+ had higher levels of RF when compared to those having Arg16+Gln27+, and patients who were carriers of Gln27 had a more active disease than non-carriers of Gln27. Our results show an association of beta2-AR SNPs with RA in a population from the northern part of Sweden. Our study also confirms the strong linkage disequilibrium of genotypes at amino acid positions 16 and 27.

Published
2004
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49. Allelic polymorphisms in the repeat and promoter regions of the interleukin-4 gene and malaria severity in Ghanaian children

Author

Gyan, B A, Goka, B, Cvetkovic, J T, Kurtzhals, J L, Adabayeri, V, Perlmann, H, Lefvert, A-K, Akanmori, B D, Troye-Blomberg, M, Gyan, B A, Goka, B, Cvetkovic, J T, Kurtzhals, J L, Adabayeri, V, Perlmann, H, Lefvert, A-K, Akanmori, B D, and Troye-Blomberg, M

Abstract

Udgivelsesdato: 2004-Oct, Immunoglobulin E has been associated with severe malaria suggesting a regulatory role for interleukin (IL)-4 and/or IgE in the pathogenesis of severe malaria. We have investigated possible associations between polymorphisms in the IL-4 repeat region (intron 3) and promoter regions (IL-4 +33CT and - 590CT) in Ghanaian children with severe malaria. There was a significantly higher frequency of IL-4 intron-3 B1B1 genotype in the cerebral malaria group [P < 0.0001, odds ratio (OR) = 8.7]. The genotype and allele frequencies of the IL-4 -590 and +33 polymorphisms did not differ between the four study groups. Carriers of IL-4 +33T/-590T with cerebral malaria had elevated total IgE compared to non-carriers (P = 0.03). Our data suggest that IL-4 and/or IgE play a regulatory role in the pathogenesis of severe or complicated malaria.

Published
2004

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