T细胞受体下调的机制及其生理意义。

D. Escors, C. Bricogne, F. Arce, G. Kochan, K. Karwacz
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引用次数: 18

摘要

有效、持久的免疫反应在很大程度上取决于T细胞的反应。抗原特异性T淋巴细胞在经过专业抗原呈递细胞(APCs)的抗原呈递后被激活并分化为效应T细胞。然而,T细胞反应受到严格调节,以防止T细胞过度激活,这可能最终导致自身免疫病理。其中一种调节机制是配体诱导的TCR下调,通过这一过程,TCR在与APC上与MHC分子相关的同源抗原肽结合后不久就从T细胞表面去除。TCR降调制是一个复杂的过程。在这里,我们简要描述了三种主要的模型,它们试图在T细胞激活和功能的背景下阐明这一机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
On the Mechanism of T cell receptor down-modulation and its physiological significance.
Effective, long-lasting immune responses largely depend upon T cell reponses. Antigen-specific T lymphocytes are activated and differentiate into effector T cells after antigen presentation by professional antigen presenting cells (APCs). However, T cell responses are tightly regulated to prevent T cell hyperactivation which may end up in autoimmune pathology. One of these regulatory mechanisms is ligand-induced TCR down-modulation, a process by which TCRs are removed from the T cell surface shortly after engagement with their cognate antigenic peptide associated to MHC molecules on the APC. TCR down-modulation is a complicated process. Here we briefly describe the three main models that attempt to clarify this mechanism in the context of T cell activation and function.
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