共刺激分子 DNAM-1 是小鼠巨细胞病毒感染期间记忆自然杀伤细胞最佳分化所必需的。
Costimulatory molecule DNAM-1 is essential for optimal differentiation of memory natural killer cells during mouse cytomegalovirus infection.
机构信息
Department of Microbiology and Immunology and the Cancer Research Institute, University of California, San Francisco, San Francisco, CA 94143, USA.
Department of Immunology, Division of Biomedical Sciences, University of Tsukuba, Ibaraki 305-8575, Japan.
出版信息
Immunity. 2014 Feb 20;40(2):225-34. doi: 10.1016/j.immuni.2013.12.011. Epub 2014 Jan 16.
Abstract
Recent studies demonstrate that natural killer (NK) cells have adaptive immune features. Here, we investigated the role of the costimulatory molecule DNAM-1 in the differentiation of NK cells in a mouse model of cytomegalovirus (MCMV) infection. Antibody blockade of DNAM-1 suppressed the expansion of MCMV-specific Ly49H(+) cells during viral infection and inhibited the generation of memory NK cells. Similarly, DNAM-1-deficient (Cd226(-/-)) Ly49H(+) NK cells exhibited intrinsic defects in expansion and differentiation into memory cells. Src-family tyrosine kinase Fyn and serine-threonine protein kinase C isoform eta (PKCη) signaling through DNAM-1 played distinct roles in the generation of MCMV-specific effector and memory NK cells. Thus, cooperative signaling through DNAM-1 and Ly49H are required for NK cell-mediated host defense against MCMV infection.
摘要
最近的研究表明，自然杀伤 (NK) 细胞具有适应性免疫特征。在这里，我们研究了在巨细胞病毒 (MCMV) 感染的小鼠模型中，共刺激分子 DNAM-1 在 NK 细胞分化中的作用。DNAM-1 的抗体阻断在病毒感染期间抑制了 MCMV 特异性 Ly49H(+)细胞的扩增，并抑制了记忆 NK 细胞的产生。同样，DNAM-1 缺陷型 (Cd226(-/-)) Ly49H(+) NK 细胞在扩增和分化为记忆细胞方面表现出内在缺陷。通过 DNAM-1 传递的Src 家族酪氨酸激酶 Fyn 和丝氨酸-苏氨酸蛋白激酶 C 同工型 eta (PKCη) 信号转导在产生 MCMV 特异性效应和记忆 NK 细胞方面发挥了不同的作用。因此，DNAM-1 和 Ly49H 的协同信号转导对于 NK 细胞介导的抗 MCMV 感染的宿主防御至关重要。
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