Self-nonself recognition by T and B lymphocytes and their roles in autoimmune phenomena.
Evidence is presented which supports the suggestion that whether a given antigen is vulnerable to an autoimmune attack is dependent upon the specific immune status of B cells and T cells to that antigen which, in turn, is dictated by the concentration of self antigen in their microenvironment. That B cells require much higher concentrations of self antigens than do T cells for the maintenance of tolerance is supported by data presented using an experimental model of acquired tolerance to serum proteins. Depending on the immune status of T cells and B cells to self antigen, the following three models are suggested for the early events leading to autoimmunity: 1) polyclonal activation of competent B cells, 2) direct activation of competent T cells, and 3) bypass of specifically tolerant T cells and activation of competent B cells. The role of a regulatory network involving the suppressor cell circuit in the induction and regulation of autoimmunity is discussed.
D000818:Animals; D001327:Autoimmune Diseases / Q000276:immunology*; D001402:B-Lymphocytes / Q000276:immunology*; D004306:Dose-Response Relationship, Immunologic; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology; D006801:Humans; D007108:Immune Tolerance; D051379:Mice; D008805:Mice, Inbred A; D011817:Rabbits; D051381:Rats; D011917:Rats, Inbred Lew; D013601:T-Lymphocytes / Q000276:immunology*; D013966:Thyroiditis / Q000276:immunology; D005719:gamma-Globulins / Q000276:immunology
D005719:gamma-Globulins