论文部分内容阅读
外周致耐有多种机制,常见一种的是失能(anergy),T细胞活化的双倍号模式表明:T细胞在识别MHC-Ag复合物的同时,如果缺乏共刺激信号的作用,就会成为失能的细胞.T细胞对实质自身抗原耐受就被认为是这样一种情况:实质细胞表面表达MHC-肽复合物,但缺乏适当的共刺激分子.识别它的T细胞就处于anegic状态.然而有一些骨髓来源的细胞,如B细胞可以在体内诱导它们所提呈抗原的耐受.这提示可能有个亚群的APC可以以一种耐受的方式提呈抗原给T细胞,从而诱导耐受,为了探讨实质性自身抗原耐受的机制是直接提呈作用呢?还是耐受性ApC相关.本文作者通过分析HA-特异的转基因CD4~+T细胞在过继输人HA~+小鼠活耐受诱导情况来证实可能的机制.
Peripheral resistance has a variety of mechanisms, a common is the loss of energy (anergy), T cell activation double pattern shows that: T cells in the recognition of MHC-Ag complex at the same time, in the absence of co-stimulatory signal effect Will become disabled cells.T cells on the real autoantigen tolerance is considered to be the case: the parenchymal cell surface expression of MHC-peptide complex, but the lack of appropriate costimulatory molecules.Recognition of its T cells in anegic However, some bone marrow-derived cells, such as B cells, can in vivo induce the tolerance of their presented antigens, suggesting that there may be a subset of APCs that can present antigens to T cells in a tolerable manner, Thereby inducing the tolerance, in order to explore whether the mechanism of substantial autoantibody tolerance is directly presented or whether it is tolerant to ApC.This study analyzed the effect of HA-specific transgenic CD4 ~ + T cells on adoptive transfer of HA ~ + Mouse survival tolerance induced situation to confirm the possible mechanism.