Studies on the autologous MLR in primary biliary cirrhosis: evidence that the autologous MLR is a negative feedblock response stimulated by activated B cells.
Patients with primary biliary cirrhosis (PBC) were found to have diminished suppression of pokeweed mitogen (PWM)-stimulated immunoglobulin synthesis by in vitro cultures containing autologous T and B cells. The possibility that this abnormality is due to a defect of autologous cell-cell interactions was suggested by the finding that patients with PBC have a significantly diminished proliferative response in the autologous mixed lymphocyte reaction (MLR). In studies of normal lymphocytes, it was found that T cells activated in the autologous MLR have the capacity to suppress PWM-stimulated immunoglobulin synthesis, but do not have augmented helper function. Furthermore, when T cells were activated with lymphoblastoid B cells, augmented suppressor activity was observed. These findings suggest that the autologous MLR represents a negative feedback loop in which activated B cells initiate a suppressor T cell pathway. The defect in the autologous MLR in patients with PBC may account for the diminished suppressor cell function observed in this disease.
D000941:Antigens / Q000276:immunology*; D001324:Autoantigens / Q000276:immunology*; D001402:B-Lymphocytes / Q000276:immunology; D005246:Feedback; D006801:Humans; D007075:Immunoglobulin M / Q000096:biosynthesis; D066298:In Vitro Techniques; D008105:Liver Cirrhosis, Biliary / Q000276:immunology*; D008213:Lymphocyte Activation; D007959:Lymphocyte Culture Test, Mixed; D011043:Pokeweed Mitogens / Q000276:immunology; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology; D050378:T-Lymphocytes, Regulatory / Q000276:immunology
D000941:Antigens; D001324:Autoantigens; D007075:Immunoglobulin M; D011043:Pokeweed Mitogens