首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >Suppression of experimental myasthenia gravis by monoclonal antibodies against MHC peptide region involved in presentation of a pathogenic T-cell epitope.
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Suppression of experimental myasthenia gravis by monoclonal antibodies against MHC peptide region involved in presentation of a pathogenic T-cell epitope.

机译:通过抗MHC肽区域的单克隆抗体抑制实验性重症肌无力,所述MHC肽区域参与致病性T细胞表位的呈递。

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摘要

We have prepared monoclonal antibodies (mAbs) against an antigen-binding region of I-A, region 62-76 of I-Abeta(b), which is involved in the T-cell participation in the pathogenesis of EAMG. The mAbs reacted with its parent molecules and inhibited the proliferation of disease-related T-cells. Passive transfer of these mAbs suppressed the occurrence of clinical EAMG, which was accompanied by decreased T-cell and Ab responses to tAChR. The results indicated that blocking the function of disease-related MHC by targeting a disease-associated region on MHC molecules could be an effective, straightforward and feasible strategy for immunointervention in MG.
机译:我们已经准备了针对I-A抗原结合区域,I-Abeta(b)62-76区域的单克隆抗体(mAb),该区域涉及T细胞参与EAMG的发病机理。 mAb与它的母体分子反应并抑制疾病相关T细胞的增殖。这些mAb的被动转移抑制了临床EAMG的发生,并伴有对tAChR的T细胞和Ab反应降低。结果表明,通过靶向MHC分子上与疾病相关的区域来阻断与疾病相关的MHC的功能可能是MG免疫干预的有效,直接和可行的策略。

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