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首页> 外文期刊>The Journal of Immunology: Official Journal of the American Association of Immunologists >Initiation of the autologous mixed lymphocyte reaction requires the expression of costimulatory molecules B7-1 and B7-2 on human peripheral blood dendritic cells.
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Initiation of the autologous mixed lymphocyte reaction requires the expression of costimulatory molecules B7-1 and B7-2 on human peripheral blood dendritic cells.

机译：自体混合淋巴细胞反应的开始需要在人外周血树突状细胞上表达共刺激分子B7-1和B7-2。

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摘要

The human autologous mixed lymphocyte reaction (AMLR) consists of a proliferative response of primarily CD4+ T lymphocytes stimulated by autologous non-T cells expressing class II MHC-encoded gene products and is thought to represent a self-recognitive mechanism that might be important in regulating the cellular interactions involved in the generation of normal immune responses. To further define appropriate stimulator cell populations, as well as the molecular mechanism responsible for the initiation of AMLR, we compared the T cell-stimulatory capacity of highly purified populations of peripheral blood dendritic cells (DCs) and monocytes (Mos) under serum-free conditions, thus carefully avoiding the presence of xenogeneic Ags. Whereas both freshly isolated Mos and DCs were found to be poor stimulators of autologous T cell proliferation, preactivation of DCs, but not of Mos, for 48 h with granulocyte-macrophage CSF led to a 113-fold increase in DC stimulatory capacity. AMLR was inhibited by mAbs against HLA-DR and CD4 molecules, and, in addition, showed a higher dependence on the granulocyte-macrophage CSF-induced up-regulation and/or de novo expression of the costimulatory molecules B7-2 and, in particular, B7-1 as compared with an Ag-specific or allogeneic MLR. Thus, our data suggest that the high density of costimulatory molecules together with MHC class II molecules on competent APCs appear to be the major triggers for the initiation of AMLR.
机译：人类自体混合淋巴细胞反应（AMLR）由表达II类MHC编码基因产物的自体非T细胞刺激的主要CD4 + T淋巴细胞的增殖反应组成，被认为代表一种自我识别机制，可能在调节参与正常免疫反应产生的细胞相互作用。为了进一步定义合适的刺激性细胞群，以及引起AMLR启动的分子机制，我们比较了无血清条件下高度纯化的外周血树突状细胞（DCs）和单核细胞（Mos）的T细胞刺激能力条件，因此要小心避免异种Ag的存在。尽管新鲜分离的Mos和DCs都是自体T细胞增殖的不良刺激物，但DCs而不是Mos的预激活作用与粒细胞巨噬细胞CSF一起作用48 h会导致DC刺激能力增加113倍。 AMLR被抗HLA-DR和CD4分子的单克隆抗体抑制，此外，对粒细胞-巨噬细胞CSF诱导的共刺激分子B7-2的上调和/或从头表达表现出更高的依赖性，B7-1与Ag特异性或同种异体MLR相比。因此，我们的数据表明，高能的共刺激分子与主管APC上的MHC II类分子一起似乎是引发AMLR的主要诱因。

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