NDLI: T cell response pattern to glutamic acid decarboxylase 65 (GAD65) peptides of newly diagnosed type 1 diabetic patients sharing susceptible HLA haplotypes

Content Provider	PubMed Central
Author	F, Rharbaoui Mayer, A. Granier, C. Bouanani, M. C, Thivolet Pau, B. J, Orgiazzi Madec, A. -m
Copyright Year	1999
Abstract	Autoantibodies and autoreactive T lymphocytes directed against several pancreatic β cell proteins such as GAD65 have been identified in the circulation before and at the onset of clinical type 1 (insulin-dependent) diabetes. Using GAD65 synthetic peptides, we studied the proliferative response of peripheral blood mononuclear cells (PBMC) either from recently diagnosed type 1 diabetic patients, of whom the majority share the disease-associated HLA class II haplotype (DR4-DQB10201 or DR3-DQB10302), or from HLA-matched control subjects. We found that 67% (14/21) of the type 1 diabetic patients and 39% (9/23) of the control subjects exhibited a positive proliferative response. Compared with control subjects, however, PBMC from diabetic patients proliferated more frequently (P < 0.05) in the presence of peptide pools from the C-terminal region of GAD65 (amino acids 379–585). Diabetic patients with the same HLA-DQ or HLA-DR alleles showed partially identical T cell reactivity, but no clear correlation could be made between MHC class II specificity and T cell epitopes because of multiple combinations of class II alleles. In addition, by flow cytometry, we studied the direct binding of GAD65 peptides to MHC class II molecules of Epstein–Barr virus (EBV)-transformed B (EBV-B) cells obtained from a diabetic patient. We found that 11 GAD peptides were able to bind to the highly susceptible haplotype DRB10301/0401-DQA10301/0501-DQB1*0302/0201 on the surface of EBV-B cells in partial correlation with the results obtained in the proliferation assays.
Related Links	http://dx.doi.org/10.1046/j.1365-2249.1999.00945.x
Starting Page	30
File Format	PDF
ISSN	13652249
e-ISSN	13652249
Journal	Clinical and Experimental Immunology
Issue Number	1
Volume Number	117
Language	English
Publisher	Blackwell Science Inc
Publisher Date	1999-07-01
Access Restriction	Open
Rights Holder	Blackwell Science Inc
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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