Defective autologous mixed lymphocyte reactivity in multiple sclerosis.
T cells from patients with multiple sclerosis (MS) and normal controls were assessed for their ability to respond in the autologous mixed lymphocyte reaction (AMLR). Cells from stable MS patients demonstrated a significant defect in their proliferative response to non-T cells in comparison to normal controls. Despite the defective AMLR response, T cells from MS patients reacted as well as T cells from normal controls to allogeneic stimuli. Furthermore, MS non-T-cells were fully capable of stimulating allogeneic MLR responses by normal and MS T cells. Since the T4+ cell is the major subpopulation which proliferates in the AMLR, these studies suggest a functional defect in a subpopulation of T4+ cells in MS patients. Since the AMLR may represent an important mechanism by which immune responses are regulated, a defect in the ability of MS T cells to respond to autologous cells could account for several of the autoimmune features of the disease.
D001327:Autoimmune Diseases / Q000276:immunology; D006801:Humans; D066298:In Vitro Techniques; D007959:Lymphocyte Culture Test, Mixed; D016685:Mitomycin; D008937:Mitomycins / Q000494:pharmacology; D008938:Mitosis; D009103:Multiple Sclerosis / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology*
D008937:Mitomycins; D016685:Mitomycin