人体抗击包括西尼罗河病毒和淋巴细胞性脉络丛脑膜炎病毒在内的RNA病毒，有赖于CD8 +T细胞介导的免疫反应。
已知RIG-I样受体（RLRs）可传递抗击RNA病毒感染的先天免疫防御系统反应信号，但其在适应性免疫中的角色尚不清楚。
本研究发现，RIG-I样受体（RLR） LGP2对于诱导先天免疫防御系统不是必须的。然而，该受体控制着抗原特异性CD8+ T细胞存活和病毒感染引起的外周血T细胞扩增。
过继转移和生化研究表明，T细胞受体信号诱导LGP2表达，而LGP2调节死亡受体信号转导并赋予细胞CD95介导细胞死亡的敏感性。
总之，LGP2促进抗原刺激引发的促生存信号，从而导致CD8 +T细胞数量的扩增和针对不同RNA病毒的抗病毒效应。(生物谷bioon.com)
doi:10.1016/j.cell.2011.10.017
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PMID:
The RIG-I-like Receptor LGP2 Controls CD8+ T Cell Survival and Fitness
Mehul S. Suthar, Hilario J. Ramos, Margaret M. Brassil, Jason Netland, Craig P. Chappell, Gabriele Blahnik, Aimee McMillan, Michael S. Diamond, Edward A. Clark, Michael J. Bevan, Michael Gale
The RIG-I-like receptors (RLRs) signal innate immune defenses upon RNA virus infection, but their roles in adaptive immunity have not been clearly defined. Here, we showed that the RLR LGP2 was not essential for induction of innate immune defenses, but rather was required for controlling antigen-specific CD8+ T cell survival and fitness during peripheral T cell-number expansion in response to virus infection. Adoptive transfer and biochemical studies demonstrated that T cell-receptor signaling induced LGP2 expression wherein LGP2 operated to regulate death-receptor signaling and imparted sensitivity to CD95-mediated cell death. Thus, LGP2 promotes an essential prosurvival signal in response to antigen stimulation to confer CD8+ T cell-number expansion and effector functions against divergent RNA viruses, including West Nile virus and lymphocytic choriomeningitis virus.
