A preliminary study of the mechanisms of immune tolerance to experimental autoimmune myasthenia gravis

AIM: To explore the mechanism of immune tolerance to experimental autoimmune myasthenia gravis (EAMG) in nasally tolerized rats and Wistar rats. METHOD: ³H]thymidine incorporation and solid-phase ELISPOT assay were used. RESULTS: The stimulative index of lymphocyte proliferation responses to acetylcholine receptor (AChR) in popliteal and inguinal lymph nodes (PILN) of EAMG rats was higher than that of nasally tolerized rats on week 3, 5 and 7 post immunization (PI) with AChR plus complete Freund's adjuvant (CFA), and was higher than that of Wistar rats on week 7 PI (P＜0.05). The values of AChR-reactive interferon(IFN)-γ-secreting cells in PILN of EAMG rats was higher than that of nasally tolerized rats and Wistar rats on week 5 and 7 PI (P＜0.05). CONCLUSIONS: When EAMG occured the lymphocyte immune response to AChR enhanced and secreting IFN-γ by Th l like cells increased. When tolerance to EAMG happened the lymphocyte immune response to AChR reduced and Thl like cells of secreting IFN-γ were suppressed.