白细胞介素-33受体ST2在小鼠巨细胞病毒感染期间可放大自然杀伤细胞的扩增并增强宿主防御。
IL-33 receptor ST2 amplifies the expansion of NK cells and enhances host defense during mouse cytomegalovirus infection.
作者信息
Nabekura Tsukasa, Girard Jean-Philippe, Lanier Lewis L
机构信息
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.
出版信息
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。
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