Tα146-162-iMDC in intervention of experimental autoimmune myasthenia graves in terms of B cell activation

To explore the mechanism of T α146-162-iMDC in intervention of experimental autoimmune myasthenia gravis (EAMG) in terms of B cell activation through use of dendritic cells pulsed with Talpha146-162 in EAMG. Thirty-four healthy male C57BL/6J mice aged 6 to 8 weeks were randomized into model group (Group A), intervention group (Group B) and control group (Group C). Dendritic cells were cultured and loaded with Tα146-162 for intervention in Group B. From initial immunization to 90th day when the experimentation was terminated, the severity of EAMG was evaluated and the morbidity was calculated. Cbl-b mRNA was detected, and Syk and Lyn protein expression and phosphorylation were assessed. Anti-AChR IgM, total IgM, IgG1, IgG2b, and IgG2c were detected on 15d, 45d and 75d after initial immunization. The morbidity of EAMG in Group A was higher than in Group B ( p 0.05). Anti-AChR IgG and IgG1 decreased in Group B compared to Group A at different time points ( p 0.05). Cbl-b suppresses secretion of subtypes of anti-AchR antibodies and B cell activation through negative regulation of B cell antigen receptor (BCR) signal pathway. Induction of B cell tolerance is a possible mechanism of intervention of T α146-162-iMDC in EAMG.