人體抗擊包括西尼羅河病毒和淋巴細(xì)胞性脈絡(luò)叢腦膜炎病毒在內(nèi)的RNA病毒，有賴于CD8 +T細(xì)胞介導(dǎo)的免疫反應(yīng),。
已知RIG-I樣受體（RLRs）可傳遞抗擊RNA病毒感染的先天免疫防御系統(tǒng)反應(yīng)信號，但其在適應(yīng)性免疫中的角色尚不清楚,。
本研究發(fā)現(xiàn),，RIG-I樣受體（RLR） LGP2對于誘導(dǎo)先天免疫防御系統(tǒng)不是必須的。然而,，該受體控制著抗原特異性CD8+ T細(xì)胞存活和病毒感染引起的外周血T細(xì)胞擴(kuò)增,。
過繼轉(zhuǎn)移和生化研究表明，T細(xì)胞受體信號誘導(dǎo)LGP2表達(dá),，而LGP2調(diào)節(jié)死亡受體信號轉(zhuǎn)導(dǎo)并賦予細(xì)胞CD95介導(dǎo)細(xì)胞死亡的敏感性。
總之,，LGP2促進(jìn)抗原刺激引發(fā)的促生存信號,，從而導(dǎo)致CD8 +T細(xì)胞數(shù)量的擴(kuò)增和針對不同RNA病毒的抗病毒效應(yīng)。(生物谷bioon.com)
doi:10.1016/j.cell.2011.10.017
PMC:
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.
