Effect of the bm12 class II mutation on proliferative and cytokine responses of encephalitogenic T cells in myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis.

摘要: The bm12 mutation in the class II I-A(b)molecule can profoundly influence experimental autoimmune disease, enhancing development of systemic lupus erythematosus-like syndromes NZB.H-2(bm12)mice or, conversely, abolishing susceptibility C57BL/6J (H-2(b)) mice to induction myasthenia gravis. We have studied effect this on encephalomyelitis (EAE), induced H-2(b)mice by myelin oligodendrocyte glycoprotein (MOG), and recently showed that MOG 35-55 peptide (pMOG 35-55), which represents immunodominant encephalitogenic region for H-2(b)mice, is also a strong encephalitogen H-2(bm12)mice. Nevertheless, although differences fine epitope specificity TCR-Vbeta gene usage between pMOG 35-55-specific T cells from H-2(b)and H-2(bm12)mice were subtle, H-2(bm12)and H-2(b)antigen presenting failed effectively cross-present non-syngeneically I-A(b)/pMOG 33-55- I-A(bm12)/pMOG cells, respectively. In present study, we show abrogation response Th1 upon non-syngeneic cross-presentation neither due cytokine shift Th2 pattern, nor result anergy induction. Therefore, suggest presentation via MHC molecule resulted ineffective stimulation, similar weak agonistic effect.