[B cell activation in experimental autoimmune myasthenia graves treated with Talpha146-162-iMDCs].

Aim: To explore the therapic effect of Talpha146-162- iMDCs in C57BL/6 mice with experimental autoimmune myasthenia graves (EAMG), and illustrate whether this therapic effect is related with the change of B cells activation.
Methods: Adult male C57BL/6 mice were randomly divided into EAMG groups(A), the prevention group(B) and control group(C); Immature bone marrow dendritic cells were cultured and pulsed with Talpha146-162. Mice of A group and B group were evaluated for clinical score till the day they were put to death. The expression and phosphorylation of Syk, Lyn, Btk and PLC-gamma2 protein were measured by Western blot.
Results: 75% mice of A group and 25% mice of B group were developed the accumulated incidence, the difference was significant (P<0.05). The average clinical score of A group and B group were 1.69+/-1.12 vs 0.35+/-0.67(P<0.01) at the termination of experiment. The expression and phosphorylation of Syk and PLC-gamma2 protein in spleen and lymphonode of the mice of A group were higher than those of C group (P<0.01) and B group (P< 0.05). Compared with C group, those of B group were higher (P<0.05); The expression and phosphorylation of Lyn protein in spleen and lymphonode of the mice of A (P<0.01) and B (P<0.05) groups were lower than those of C group. Compared with A group, those of B group were higher (P<0.05); The expression of Btk protein in spleen and lymphonode of the mice of A (P<0.01) and B (P<0.05) groups were higher than those of C group. And those of B groups were lower than those of A group (P<0.05). But there were no remarkable differences among the phosphorylation of Btk protein of three groups.
Conclusion: Talpha146-162-iMDCs can prevent EAMG and probably ameliorate EAMG by the negative regulation on BCR signaling.