Nabekura Tsukasa, Girard Jean-Philippe, Lanier Lewis L
Department of Microbiology and Immunology and the Cancer Research Institute, University of California, San Francisco, San Francisco, CA 94143; Life Science Center of Tsukuba Advanced Research Alliance, University of Tsukuba, Ibaraki 305-8577, Japan; and.
Centre National de la Recherche Scientifique and Université de Toulouse, Institut de Pharmacologie et de Biologie Structurale, F-31077 Toulouse, France.
J Immunol. 2015 Jun 15;194(12):5948-52. doi: 10.4049/jimmunol.1500424. Epub 2015 Apr 29.
NK cells provide important host defense against viruses and can differentiate into self-renewing memory NK cells after infection, alloantigen stimulation, and cytokine stimulation. In this study, we investigated the role of the IL-33 receptor ST2 in the differentiation of NK cells during mouse CMV (MCMV) infection. Although ST2-deficient (Il1rl1 (-/-)) Ly49H(+) NK cells develop normally and differentiate into memory cells after MCMV infection, naive and memory Il1rl1 (-/-) Ly49H(+) NK cells exhibited profound defects in MCMV-specific expansion, resulting in impaired protection against MCMV challenge. Additionally, IL-33 enhanced m157 Ag-specific proliferation of Ly49H(+) NK cells in vitro. Thus, an IL-33/ST2 signaling axis in NK cells contributes to host defense against MCMV.
自然杀伤（NK）细胞为宿主抵御病毒提供重要防御，并且在感染、同种异体抗原刺激和细胞因子刺激后可分化为自我更新的记忆性NK细胞。在本研究中，我们调查了白细胞介素-33（IL-33）受体ST2在小鼠巨细胞病毒（MCMV）感染期间NK细胞分化中的作用。尽管ST2缺陷型（Il1rl1 (-/-)）Ly49H(+) NK细胞正常发育，并在MCMV感染后分化为记忆细胞，但未成熟和记忆性Il1rl1 (-/-) Ly49H(+) NK细胞在MCMV特异性扩增方面表现出严重缺陷，导致对MCMV攻击的保护受损。此外，IL-33在体外增强了Ly49H(+) NK细胞的m157抗原特异性增殖。因此，NK细胞中的IL-33/ST2信号轴有助于宿主抵御MCMV。
