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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 >Presentation by myoblasts of an epitope from endogenous acetylcholine receptor indicates a potential role in the spreading of the immune response.
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Presentation by myoblasts of an epitope from endogenous acetylcholine receptor indicates a potential role in the spreading of the immune response.

机译:成肌细胞呈递来自内源性乙酰胆碱受体的表位表明在免疫应答扩散中的潜在作用。

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摘要

It is generally considered that myoblasts are unable to prime naive T cell responses without help from professional antigen-presenting cells (APC). However, their ability to present endogenous antigens to previously primed T lymphocytes in the secondary phase of a T cell response has not been well studied. We show here that primary human myoblasts, when stimulated with IFNgamma to express class II MHC, can present an endogenous epitope, probably an acetylcholine receptor (AChR) peptide, to a CD4(+) AChR-specific T helper lymphocyte clone. Presentation leads to secretion of IFNgamma by the T cell clone and, in addition, killing of the myoblast. Our results suggest that, during the effector phase of the immune response, myoblasts could enhance the inflammatory response by presenting endogenous antigen, and thereby become targets for CD4(+) T lymphocyte-induced cytotoxicity; subsequent release of myoblast antigens could then lead to inter- and intra-molecular determinant spreading.
机译:通常认为成肌细胞在没有专业抗原呈递细胞(APC)的帮助下无法引发幼稚T细胞反应。然而,尚未充分研究它们在T细胞应答的第二阶段将内源性抗原呈递给先前引发的T淋巴细胞的能力。我们在这里显示,原人类成肌细胞,当用IFNgamma刺激表达II类MHC时,可以向CD4(+)AChR特异性T辅助淋巴细胞克隆呈现内源性表位,可能是乙酰胆碱受体(AChR)肽。呈递导致T细胞克隆分泌IFNγ,此外,杀死成肌细胞。我们的研究结果表明,在免疫应答的效应期,成肌细胞可以通过呈递内源性抗原来增强炎症反应,从而成为CD4(+)T淋巴细胞诱导的细胞毒性的靶标。随后,成肌细胞抗原的释放可能导致分子间和分子内决定簇扩散。

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