Effect of agonist CD40 monoclonal antibody on the tolerance of experimental autoimmune myasthenia gravis
10.3760/cma.j.issn.1671-8925.2011.02.009
- VernacularTitle:激发型CD40单克隆抗体对实验性自身免疫性重症肌无力耐受的影响
- Author:
Luo-Qing LI
1
;
Sheng-Gang SUN
;
Xue-Bing CAO
;
Yun-Fu WANG
Author Information
1. 湖南省岳阳市一人民医院
- Keywords:
Myasthenia gravis;
Immunotolerance;
Antigen,CD40;
Dendritic cell;
Monoclonal antibody
- From:
Chinese Journal of Neuromedicine
2011;10(2):151-154
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of agonist CD40 monoclonal antibody (CD40mAb) on the tolerance of experimental autoimmune myasthenia gravis (EAMG) induced by immature dendritic cells (iDCs). Methods Lewis rats were equally randomized into normal group,EAMG group, tolerance group and CD40mAb treatment group (n=5). Rats in the tolerance group and CD40mAb treatment group were vaccinated with AChR pulsed iDCs; and rats in the CD40mAb treatment group were intraperitoneally injected CD40mAb at a dosage of 0.5 mg once when performing the vaccination and on the 2rd d of vaccination. One mL serum-free medium was given to the rats in the EAMG group; normal group did not receive any treatment. Three weeks after that, rats in the above 4 groups were immunized with AChR and complete Freund's adjuvant (CFA). Seven weeks after the immunization, the corresponding indexes of MG were observed: behavioral assessment was performed and electromyogram was employed to detect the repetitive nerve stimulation on these rats; enzyme-linked immunosorbent assay (ELISA) was used to determine the level of AChRab; the pathological changes of neuromuscular junction were also detected. Results Just as the rats in the normal group, the rats in the tolerance group did not have significant changes in any of the corresponding indexes of MG after being immunized with AChR and CFA. In contrast, rats in both EAMG group and CD40mAb treatment group showed typical changes in the corresponding indexes of MG: their electromyogram wave amplitude obviously attenuated; the level of serum AChRab increased and neuromuscular junction appeared as a typical damage of MG. Conclusion Agonist CD40mAb could abrogate the tolerance of EAMG induced by AChR pulsed iDCs, suggesting that the dysfunction of DCs is related to the priming of abnormal immune of MG.
