重症肌无力患者FOXP3表达变化与体液免疫异常的相关性

来源 :中国神经免疫学和神经病学杂志 | 被引量 : 0次 | 上传用户:llt009
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目的探讨重症肌无力(MG)患者外周血叉头样转录因子P3(FOXP3)表达变化与体液免疫异常的关系。方法利用RT-PCR技术检测41例MG患者和20名体检健康者外周血单个核细胞FOXP3、B淋巴细胞激活因子(BLyS)、补体调节因子膜反应性溶解抑制物(CD59)和衰变加速因子(DAF)的mRNA表达,用ELISA法检测外周血清转化生长因子(TGF-β1)、抗乙酰胆碱受体抗体(anti-AChR-IgG)水平,并进一步分析其间的关系。结果(1)MG患者组外周血FOXP3、CD59、DAF的mRNA表达及血清TGF-β1水平明显低于健康对照组,BlySmRNA表达水平明显高于健康对照组(均P<0.01);(2)外周血FOXP3、BLyS、CD59、DAF的mRNA表达及血清TGF-β1水平,在眼肌型与全身型MG患者间差异无统计学意义;(3)41例MG患者中血清抗AChR-IgG阳性30例,眼肌型(18例)和全身型(12例)血清抗AChR-IgG水平差异无统计学意义(P>0.05);(4)MG组外周血单个核细胞FOXP3 mRNA表达与血清TGF-β1水平及CD59、DAF mRNA表达水平呈正相关(分别r=0.84,P<0.01;r=0.455,P<0.05;r=0.435,P<0.05),与BLyS mRNA表达呈负相关(r=-0.58,P<0.05);血清抗AChR-IgG抗体阳性患者中,抗AChR-IgG抗体水平与FOXP3 mRNA表达水平、血清TGF-β1水平呈负相关(分别r=-0.77、r=-0.81,均P<0.01),而与BLyS mRNA表达水平呈正相关(r=0.757,P<0.01),与CD59、DAF mRNA水平无相关性(P>0.05)。结论 FOXP3 mRNA、TGF-β1低表达可能促进B细胞活化,进而通过增加AChR抗体产生及抑制补体调节蛋白活化促进体液免疫,在MG发病中起重要作用。 Objective To investigate the relationship between the expression of Fork-like transcription factor P3 (FOXP3) and humoral immunity in patients with myasthenia gravis (MG). Methods RT-PCR was used to detect the expression of FOXP3, B lymphocyte activation factor (BLyS), CD59 and decay accelerating factor (CD59) in peripheral blood mononuclear cells of 41 patients with MG and 20 healthy subjects. DAF) were detected by enzyme linked immunosorbent assay (ELISA). The levels of TGF-β1 and anti-AChR-IgG in peripheral blood were detected by ELISA. Results (1) The mRNA expression of FOXP3, CD59 and DAF and the level of serum TGF-β1 in peripheral blood of MG patients were significantly lower than those in healthy controls (P <0.01) The mRNA expression of FOXP3, BLyS, CD59, DAF and the level of serum TGF-β1 were not statistically different between patients with ocular muscle and those with systemic MG. (3) Serum anti-AChR-IgG positive in 30 MG patients (P> 0.05). (4) The expression of FOXP3 mRNA in peripheral blood mononuclear cells of MG group was not significantly different from that of serum TGF-β1 (R = -0.58, P <0.05, r = 0.435, P <0.05), but negatively correlated with the expression of BLyS mRNA (r = -0.58, There was a negative correlation between the level of FOXP3 mRNA and the level of serum TGF-β1 (r = -0.77, r = -0.81, P <0.05, respectively), but not in AChR-IgG positive patients 0.01), but positively correlated with the level of BLyS mRNA (r = 0.757, P <0.01), but not with the levels of CD59 and DAF mRNA (P> 0.05). Conclusion The low expression of FOXP3 mRNA and TGF-β1 may promote the activation of B cells, and then promote the humoral immunity by increasing the production of AChR antibody and inhibiting the activation of complement regulatory protein, which play an important role in the pathogenesis of MG.
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