Laboratory of Molecular Immunology, Infectious and Inflammatory Diseases Center, Sanford Burnham Medical Research Institute, 10901 N. Torrey Pines Road, La Jolla, CA 92037, USA.
Curr Opin Immunol. 2011 Oct;23(5):627-31. doi: 10.1016/j.coi.2011.08.008. Epub 2011 Sep 13.
The herpesvirus entry mediator (HVEM; TNFRSF14) can activate either proinflammatory or inhibitory signaling pathways. HVEM engages two distinct types of ligands, the canonical TNF-related cytokines, LIGHT and Lymphotoxin-α, and the Ig-related membrane proteins, BTLA (B and T lymphocyte attenuator) and CD160. Recent evidence indicates that the signal generated by HVEM depends on the context of its ligands expressed in trans or in cis. HVEM engagement by all of its ligands in trans initiates bidirectional signaling. In contrast, naïve T cells coexpress BTLA and HVEM forming a cis-complex that interferes with the activation of HVEM by extraneous ligands in the surrounding microenvironment. The HVEM Network is emerging as a key survival system for effector and memory T cells in mucosal tissues.
疱疹病毒进入介体 (HVEM; TNFRSF14) 可以激活促炎或抑制信号通路。HVEM 与两种不同类型的配体结合,即经典的 TNF 相关细胞因子 LIGHT 和淋巴毒素-α,以及 Ig 相关膜蛋白 BTLA(B 和 T 淋巴细胞衰减器)和 CD160。最近的证据表明,HVEM 产生的信号取决于其在转位或顺式中表达的配体的上下文。HVEM 与其所有配体在转位上的结合会引发双向信号。相比之下,幼稚 T 细胞共表达 BTLA 和 HVEM,形成顺式复合物,干扰周围微环境中外源配体对 HVEM 的激活。HVEM 网络正成为粘膜组织中效应器和记忆 T 细胞的关键存活系统。