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首页> 外文期刊>Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society >Activation-induced accumulation of B and T lymphocyte attenuator at the immunological synapse in CD4+ T cells
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Activation-induced accumulation of B and T lymphocyte attenuator at the immunological synapse in CD4+ T cells

机译：在CD4 + T细胞的免疫突触中活化诱导的B和T淋巴细胞减毒剂的积累

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摘要

BTLA, a recently cloned coreceptor expressed on lymphocytes, negatively regulates cell activation by recruiting SHP-1/SHP-2. However, the mechanisms that regulate the intracellular localization of BTLA and its trafficking to the cell surface in T cells are still unknown. To determine the mechanisms that regulate the expression of BTLA on the surface of T cells, we examined the subcellular localization of BTLA in mouse T cells in a steady state, as well as upon activation by using a confocal laser-scanning microscopy. We found that BTLA was localized mainly in the Golgi apparatus and secretory lysosomes in resting CD4+ T cells. We also found that intracellular BTLA was translocated to the cell surface and accumulated at the immunological synapse upon TCR stimulation. Furthermore, we found that the BTLA-HVEM interaction was required for the association of BTLA with lipid rafts. These results indicate that the surface expression of BTLA and its accumulation at the immunological synapse are tightly regulated by TCR and HVEM stimulation to deliver efficient inhibitory signals in the regulation of CD4+ T cell activation.
机译：BTLA是最近在淋巴细胞上表达的一种克隆的共受体，通过募集SHP-1 / SHP-2负调节细胞活化。但是，调节BTLA的细胞内定位及其向T细胞中细胞表面运输的机制仍然未知。为了确定调节BTLA在T细胞表面表达的机制，我们检查了BTLA在小鼠T细胞中的亚细胞定位（在稳态下）以及通过使用共聚焦激光扫描显微镜激活后的状态。我们发现BTLA主要定位于高尔基体和静息CD4 + T细胞中的分泌溶酶体。我们还发现细胞内BTLA易位到细胞表面并在TCR刺激后在免疫突触处积累。此外，我们发现BTLA-HVEM相互作用是BTLA与脂质筏的结合所必需的。这些结果表明，BTLA的表面表达及其在免疫突触中的积累受到TCR和HVEM刺激的严格调控，从而在CD4 + T细胞活化的调控中传递有效的抑制信号。

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