白介素-12、23亚单位在重症肌无力发病中的作用

Effect of interleukin-12,23 subunits in the pathogenesis of myasthenia gravis

目的探讨白介素(IL)-12、23亚单位在重症肌无力(MG)发病中的作用。方法采用RT-PCR及ELISA法分别测定22例MG患者(全身型12例,眼肌型10例)和22名健康体检者外周血单个核细胞(PBMCs)中IL-12p35、IL-23p19及p40(IL-12/23)mRNA的表达及血清抗乙酰胆碱受体(AChR)抗体、干扰素(IFN)-γ和IL-17水平,并进行相关性分析。结果 (1)MG组PBMCs中IL-12p35、IL-23p19和p40(IL-12/23)mRNA表达及其血清IFN-γ和IL-17水平明显高于正常对照组(P<0.05～0.01);但MG全身型亚组和眼肌型亚组间差异无统计学意义。(2)MG组血清抗AChR-IgG阳性17例,抗AChR-IgG水平与其IL-12p35、IL-23p19和p40(IL-12/23)mRNA表达及血清IFN-γ和IL-17水平均呈正相关(r=0.502、0.649、0.817、0.652、0.484,P<0.05～0.01)。(3)MG组IL-12p35mRNA与IFN-γ、IL-23p19mRNA与IL-17均呈正相关(r=0.906、0.725,均P<0.01)。结论 IL-12和IL-23可能分别通过促进IFN-γ和IL-17的分泌参与了MG的发病,但与MG类型无关。

Objective To explore the effect of interleukin（IL）-12,23 subunits in the pathogenesis of myasthenia gravis （MG）.Methods The expression of IL-12p35,IL-23p19 and p40（IL-12/23） mRNA in peripheral blood mononuclear cells （PBMCs） and the levels of serum anti-acetylcholine receptor（AChR）-IgG,interferon-gamma（IFN）-γ and IL-17 were detected by RT-PCR and ELISA in 22 MG patients（including 12 cases of general type and 10 cases of ocular type）and 22 healthy controls,and the correlation among them were analyzed.Results （1） The expression of IL-12p35,IL-23p19 and p40 （IL-12/23） mRNA in PBMCs and the serum IFN-γ and IL-17 concentration in MG group were significantly higher than those in the normal control group （P0.05-0.01）; but there was no statistically significant between the MG general type subgroup and MG ocular type subgroup. （2） The serum anti-AChR-IgG were positive in 17 MG patients,and the level was positive correlated with the expression of IL-12p35,IL-23p19,p40 （IL-12/23） mRNA and serum IFN-γ and IL-17 concentrations （r=0.502,0.649,0.817,0.652,0.484;P0.05-0.01）. （3） The expression of IL-12p35 mRNA and IL-23p19 mRNA were positive correlated with IFN-γ,IL-17,respectively （r=0.906,0.725;all P0.01）. Conclusion IL-12 and IL-23 may participate MG pathogenesis by promoting IFN-γ and IL-17 secretion respectively,but they probably have no correlations with MG type.