Suppressive effect of glutamic acid decarboxylase 65-specific autoimmune B lymphocytes on processing of T cell determinants located within the antibody epitope

Journal of Immunology

Volumn 169, Issue 2, 2002, Pages 665-672

  Jaume, Juan Carlos ^a   Parry, Sarah Louise ^a   Madec, Anne Marie ^a   Sønderstrup, Grete ^a   Baekkeskov, Steinunn ^a  

^a UNIVERSITY OF CALIFORNIA   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

AUTOANTIGEN; EPITOPE; GLUTAMATE DECARBOXYLASE; GLUTAMATE DECARBOXYLASE 65; HLA DR ANTIGEN; UNCLASSIFIED DRUG;

ANTIBODY PRODUCTION; ANTIGEN ANTIBODY COMPLEX; ANTIGEN PRESENTATION; ANTIGEN PRESENTING CELL; ANTIGEN SPECIFICITY; ARTICLE; AUTOIMMUNITY; B LYMPHOCYTE; HUMAN; HUMAN CELL; HYBRIDOMA; IMMUNE DEFICIENCY; IMMUNOMODULATION; INSULIN DEPENDENT DIABETES MELLITUS; PRIORITY JOURNAL; SPLEEN CELL; T LYMPHOCYTE;

EID: 0037100387     PISSN: 00221767     EISSN: None     Source Type: Journal    
DOI: 10.4049/jimmunol.169.2.665     Document Type: Article

References (28)

1. Antigen uptake and accumulation in antigen-specific B cells
2. Antigen presentation by non-immune B-cell hybridoma clones: Presentation of synthetic antigenic sites reveals clones that exhibit no specificity and clones that present only one epitope
3. Endocrine autoimmunity
4. Thyroid peroxidase autoantibody fingerprints in hypothyroid and euthyroid individuals. I. Cross-sectional study in elderly women
5. r islet cell protein after onset of type 1 diabetes
6. Does GAD have a unique role in triggering IDDM?
7. null mice
8. Direct evidence for the contribution of B cells to the progression of insulitis and the development of diabetes in non-obese diabetic mice
9. B lymphocytes are critical antigen-presenting cells for the initiation of T cell-mediated autoimmune diabetes in nonobese diabetic mice
10. B lymphocytes are crucial antigen-presenting cells in the pathogenic autoimmune response to GAD65 antigen in nonobese diabetic mice
11. I-Ag7-mediated antigen presentation by B lymphocytes is critical in overcoming a checkpoint in T cell tolerance to islet β cells of nonobese diabetic mice
12. B cell specificity contributes to the outcome of diabetes in nonobese diabetic mice
13. Development of type 1 diabetes despite severe hereditary B-lymphocyte deficiency
14. Closing in on type 1 diabetes
15. Suppressive effect of antibody on processing of T cell epitopes
16. Modulation of antigen processing by bound antibodies can boost or suppress class II major histocompatibility complex presentation of different T cell determinants
17. IgG Fc receptors
18. GAD65-specific autoantibodies enhance the presentation of an immunodominant T-cell epitope from GAD65
19. Enhancing or suppressive effects of antibodies on processing of a pathogenic T cell epitope in thyroglobulin
20. High-resolution autoreactive epitope mapping and structural modeling of the 65 kDa form of human glutamic acid decarboxylase
21. Four IgG anti-islet human monoclonal antibodies isolated from a type 1 diabetes patient recognize distinct epitopes of glutamic acid decarboxylase 65 and are somatically mutated
22. Identification of immunodominant T cell epitopes of human glutamic acid decarboxylase 65 by using HLA-DR (α1*0101, β1*0401) transgenic mice
23. Naturally processed T cell epitopes from human glutamic acid decarboxylase identified using mice transgenic for the type 1 diabetes-associated human MHC class II allele, DRB1*0401
24. High prevalence of GAD65 (and IA-2) antibodies in Japanese IDDM patients by a new immunoprecipitation assay based on recombinant human GAD65
25. Structure of the human class I histocompatibility antigen, HLA-A2
26. Visualization of peptide-specific T cell immunity and peripheral tolerance induction in vivo
27. Differential presentation of glutamic acid decarboxylase 65 (GAD65) T cell epitopes among HLA-DRB10401-positive individuals
28. Identification of naturally processed T cell epitopes from glutamic acid decarboxylase presented in the context of HLA-DR alleles by T lymphocytes of recent onset IDDM patients