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首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >Myocytes respond in vivo to an antibody reactive with the acetylcholine receptor by upregulating interleukin-15: an interferon-gamma activator with the potential to influence the severity and course of experimental myasthenia gravis.
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Myocytes respond in vivo to an antibody reactive with the acetylcholine receptor by upregulating interleukin-15: an interferon-gamma activator with the potential to influence the severity and course of experimental myasthenia gravis.

机译:心肌细胞通过上调白介素15(一种可能影响实验性重症肌无力的严重程度和病程的潜力)的白介素15来对与乙酰胆碱受体具有反应性的抗体产生体内反应。

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摘要

The monoclonal antibody, mAb35, which binds the main immunogenic region of the post-junctional muscle receptor for acetylcholine (AChR), results in contractile dysfunction and symptoms of experimental myasthenia gravis (EAMG). As described below, exposure to mAb35 also results in the production by muscle of increased levels of the interferon-gamma (IFN-gamma)-activating cytokine, interleukin-15. This effect is accompanied by the increased trafficking of leukocytes through muscle, some that produce IFN-gamma. These observations may be relevant to the induction of disease symptoms since numerous reports from other investigators indicate that IFN-gamma may play a pivotal role in this disease process.
机译:单克隆抗体mAb35与乙酰胆碱(AChR)的连接后肌肉受体的主要免疫原性区域结合,导致收缩功能障碍和实验性重症肌无力(EAMG)的症状。如下所述,暴露于mAb35也会导致肌肉产生增加水平的干扰素-γ(IFN-γ)激活细胞因子白介素15。这种作用伴随着白细胞通过肌肉的运输增加,其中一些产生IFN-γ。这些观察结果可能与疾病症状的诱导有关,因为其他研究者的大量报告表明,IFN-γ可能在该疾病过程中起关键作用。

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