T- and B-cell interactions in autoimmune syndromes.
We have reviewed briefly some of the individual capabilities of T and B cells and how these can be modified by interactions between the two cell lines. Evidence that T cells have their own distinct receptors for antigens, yet under certain circumstances may bind IgM or IgG produced by B cells, has been particularly emphasized. The probability that B cells, in turn, may bind the antigen receptor of T-cell origin reflects the balanced nature of an intricate communication system in which interactions between antigens, antigen receptors, and binding sites for these receptors all serve to modulate the integrated functioning of T and B cells. It is suggested that this communication system is disturbed in patients with rheumatoid arthritis; specifically, it is proposed that defective feedback activity of IgG-antigen complexes on activated T cells may exist in some patients and could result in unchecked and harmful T-cell activity in the joint. Therapeutic implications of this idea are mentioned.
D000818:Animals; D000917:Antibody Formation; D000936:Antigen-Antibody Complex; D000937:Antigen-Antibody Reactions; D001172:Arthritis, Rheumatoid / Q000276:immunology; D001323:Autoantibodies; D001327:Autoimmune Diseases / Q000276:immunology*; D001402:B-Lymphocytes / Q000276:immunology*; D001666:Binding Sites, Antibody; D002645:Chickens; D006801:Humans; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D051379:Mice; D012217:Rheumatoid Factor; D013601:T-Lymphocytes / Q000276:immunology*
D000936:Antigen-Antibody Complex; D001323:Autoantibodies; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D012217:Rheumatoid Factor