疱疹病毒侵入介体在免疫应答及抗肿瘤免疫中的研究进展

Herpesvirus entry mediator:a switch in immune response and its role in anti-tumor immunity

T细胞以及抗原提呈细胞上的受体和它们的配体所传递的激活或抑制信号,对于免疫细胞的有效激活或保持休眠状态极其重要。肿瘤坏死因子受体超家族和CD28-B7家族就包含了很多这样的调节分子。疱疹病毒侵入介体(HVEM)能在其配体肿瘤坏死因子超家族成员14(LIGHT)的作用下参与细胞免疫应答的激活;同时HVEM作为B和T淋巴细胞衰减子(BTLA)的配体,使其转导共抑制信号。本文介绍HVEM精细调节免疫的功能并讨论其在抗肿瘤免疫中的新进展。

The interaction between co-stimulatory ligands and their receptors of T cells and antigen presenting cells is crucial for the activation or resting of the immune cells. The tumor necrosis factor receptor superfamily and CD28-B7 family contain many such regulatory molecules. Herpesvirus entry mediator （HVEM）, also named as tumor necrosis factor superfamily member 14, is noted for its pivotal role in regulating immune responses through binding LIGHT as a ligand to develop T-cell immunity, and in interacting with B and T lymphocyte attenuator（BTLA） as a receptor to negatively regulate T-cell responses. In antitumor immunity, increasing amount of evidence demonstrates that HVEM is an indispensable receptor on lymphocyte for LIGHT to co-stimulate tumor antigen-specific CTL. This article discusses the role of HVEM in regulating immune response and antitumor-immunity.