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目的 :研究CD40配体在血清阳性重症肌无力 (SPMG)和血清阴性重症肌无力 (SNMG)主要致病因素产生中的作用。结果 :无论SPMG或SNMG ,外周血单个核细胞体外培养后上清液中γ干扰素 (IFN γ)、白细胞介素 4(IL 4)、抗乙酰胆碱受体抗体 (AChRab)和抗突触前膜受体抗体 (Prsmab)均比健康对照组非常显著增高 (P =0 0 0 0 )。抗CD40L单克隆抗体 (anti CD40Lmonoclonalantibody ,CD40LMcAb)干预后 ,SPMG组与健康对照组的差异无统计学意义 (P >0 0 5 ) ,SNMG组只有PsmRab与健康对照组的差异无统计学意义 (P >0 0 5 ) ,而IFN γ、IL 4和AChRab的水平虽有所下降 ,但仍显著高于健康对照组 (P <0 0 5 )。结论 :SNMG的AChRab、IFN γ和IL 4可能还通过其他途径产生 ,存在其他发病机制。
AIM: To investigate the role of CD40 ligands in the production of the major causative agents of seronegative myasthenia gravis (SPMG) and seronegative myasthenia gravis (SNMG). Results: The expression of IFN-γ, IL-4, AChRab and anti-presynaptic membrane protein in supernatant of peripheral blood mononuclear cells were detected by SPMG or SNMG in vitro. Receptor antibody (Prsmab) were significantly higher than the healthy control group (P = 0 0 0). There was no significant difference between SPMG group and healthy control group after anti-CD40L monoclonal antibody (CD40LMcAb) intervention (P> 0.05). There was no significant difference between PsmRab group and healthy control group in SNMG group (P > 0 0 5), while the levels of IFN γ, IL 4 and AChRab were still significantly lower than those of healthy controls (P <0.05). Conclusion: AChRab, IFNγ and IL-4 of SNMG may also be produced by other pathways, and other pathogenesis exists.