Objective: To explore the therapeutic effect of Talpha146-162-iMDCs on C57BL/6 mice with EAMG and the role of changes in B cell activation regulated by Cbl.
Methods: Thirty four adult male C57BL/6 mice were randomly divided into EAMG group (A group), EAMG group with interventions (B group) and control group (C group). T-AChR antigens were injected to the mice in A and B groups to induce EAMG. Meanwhile, dendritic cells from immature bone marrows were cultured and pulsed with Talpha146-162, and injected to the mice in the intervention group. The mRNA expression of Cbl was detected by RT-PCR 90 days after the termination of experiment. The expression and phosphorylation of Syk and Lyn proteins were measured by Western blot.
Results: More mice (9/12, 75%) in A group developed EAMG than in B group (3/12, 25%, P<0.05). Mice in A group also suffered more serious illness in terms of clinical scores than mice in B group (1.69+/-1.12 vs 0.35+/-0.67, P<0.01). No EAMG occurred in mice in C group. Mice in B group had lower mRNA expressions of Cbl in the spleens and lymphonodes than mice in A groups, but both had higher expressions than mice in C group (P<0.05). Mice in B group had higher mRNA expression of Cbl than mice in A group (P<0.05).
Conclusion: Talpha146-162-iMDCs prevent EAMG, possibly through negative regulation of Cbl on BCR signaling.