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B cells produce less IL-10, IL-6 and TNF-alpha in myasthenia gravis

机译:B细胞在重症肌无力中产生较少的IL-10,IL-6和TNF-α

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B cells from myasthenia gravis (MG) patients with autoantibodies (Aab) against acetylcholine receptor (AChR), muscle-specific kinase (MuSK) or with no detectable Aab were investigated as cytokine producing cells in this study. B cells were evaluated for memory phenotypes and expressions of IL-10, IL-6 and IL-12A. Induced productions of IL-10, IL-6, IL-12p40, TNF-alpha and LT from isolated B cells in vitro were measured by immunoassays. MG patients receiving immunosuppressive treatment had higher proportions of memory B cells compared with healthy controls and untreated patients. With CD40 stimulation MG patients produced significantly lower levels of IL-10, IL-6. With CD40 and B cell receptor stimulation of B cells, TNF-alpha production also decreased in addition to these cytokines. The lower levels of these cytokine productions were not related to treatment. Our results confirm a disturbance of B cell subpopulations in MG subgroups on immunosuppressive treatment. B cell derived IL-10, IL-6 and TNF-alpha are down-regulated in MG, irrespective of different antibody productions. Ineffective cytokine production by B cells may be a susceptibility factor in dysregulation of autoimmune Aab production.
机译:在这项研究中,研究了重症肌无力(MG)患者的B细胞具有针对乙酰胆碱受体(AChR),肌肉特异性激酶(MuSK)或没有可检测到的Aab的自身抗体(Aab)作为细胞因子产生细胞。评估B细胞的记忆表型和IL-10,IL-6和IL-12A的表达。通过免疫测定测量了体外分离的B细胞诱导的IL-10,IL-6,IL-12p40,TNF-α和LT的产生。与健康对照组和未经治疗的患者相比,接受免疫抑制治疗的MG患者的记忆B细胞比例更高。通过CD40刺激,MG患者产生的IL-10,IL-6水平明显降低。通过B细胞的CD40和B细胞受体刺激,除这些细胞因子外,TNF-α的产生也​​降低了。这些细胞因子产生的较低水平与治疗无关。我们的结果证实了免疫抑制治疗对MG亚组B细胞亚群的干扰。 MG中下调了B细胞来源的IL-10,IL-6和TNF-α,而与产生不同的抗体无关。 B细胞产生的无效细胞因子可能是自身免疫Aab产生失调的易感因素。

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