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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Triggering receptor expressed on myeloid cell-like transcript 2 (TLT-2) is a counter-receptor for B7-H3 and enhances T cell responses
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Triggering receptor expressed on myeloid cell-like transcript 2 (TLT-2) is a counter-receptor for B7-H3 and enhances T cell responses

机译：髓样细胞样转录物2（TLT-2）上表达的触发受体是B7-H3的反受体，可增强T细胞反应

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摘要

The B7 family member B7-H3 (CD276) plays important roles in immune responses. However, the function of B7-H3 remains controversial. We found that murine B7-H3 specifically bound to Triggering receptor expressed on myeloid cells (TREM)-like transcript 2 (TLT-2, TREML2). TLT-2 was expressed on CD8~+ T cells constitutively and on activated CD4~+ T cells. Stimulation with B7-H3 transfectants preferentially up-regulated the proliferation and IFN-γ production of CD8~+ T cells. Transduction of TLT-2 into T cells resulted in enhanced IL-2 and IFN-γ production via interactions with B7-H3. Blockade of the B7-H3:TLT-2 pathway with a mAb against B7-H3 or TLT-2 efficiently inhibited contact hypersensitivity responses. Our results demonstrate a direct interaction between B7-H3 and TLT-2 that preferentially enhances CD8~+ T cell activation.
机译：B7家族成员B7-H3（CD276）在免疫反应中起重要作用。但是，B7-H3的功能仍存在争议。我们发现，鼠B7-H3与髓样细胞（TREM）样转录本2（TLT-2，TREML2）上表达的触发受体特异性结合。 TLT-2在CD8〜+ T细胞上组成性表达，在活化的CD4〜+ T细胞上表达。 B7-H3转染子的刺激优先上调CD8〜+ T细胞的增殖和IFN-γ的产生。通过与B7-H3相互作用，将TLT-2转导至T细胞导致IL-2和IFN-γ产生增加。用针对B7-H3或TLT-2的mAb阻断B7-H3：TLT-2途径可有效抑制接触超敏反应。我们的结果表明B7-H3与TLT-2之间存在直接相互作用，从而优先增强CD8〜+ T细胞的活化。

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