期刊
JOURNAL OF LEUKOCYTE BIOLOGY
卷 89, 期 4, 页码 517-523出版社
FEDERATION AMER SOC EXP BIOL
DOI: 10.1189/jlb.0910528
关键词
costimulation; coinhibition; pathogenesis
资金
- National Institutes of Health [RO1 AI061516, F32 DK082249]
- Crohn's and Colitis Foundation of America
The HVEM, or TNFRSF14, is a membrane-bound receptor known to activate the NF-kappa B pathway, leading to the induction of proinflammatory and cell survival-promoting genes. HVEM binds several ligands that are capable of mediating costimulatory pathways, predominantly through its interaction with LIGHT (TNFSF14). However, it can also mediate coinhibitory effects, predominantly by interacting with IGSF members, BTLA or CD160. Therefore, it can function like a molecular switch for various activating or inhibitory functions. Furthermore, recent studies suggest the existence of bidirectional signaling with HVEM acting as a ligand for signaling through BTLA, which may act as a ligand in other contexts. Bidirectional signaling, together with new information indicating signaling in cis by cells that coexpress HVEM and its ligands, makes signaling within a HVEM-mediated network complicated, although potentially rich in biology. Accumulating in vivo evidence has shown that HVEM-mediated, coinhibitory signaling may be dominant over HVEM-mediated costimulatory signaling. In several disease models the absence of HVEM-BTLA signaling predominantly resulted in severe mucosal inflammation in the gut and lung, autoimmune-like disease, and impaired immunity during bacterial infection. Here, we will summarize the current view about how HVEM-BTLA signaling is involved in the regulation of mucosal inflammation, autoimmunity, and infection immunity. J. Leukoc. Biol. 89: 517-523; 2011.
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