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前沿:杀伤细胞凝集素样受体G1分子在小鼠自然杀伤细胞激活过程中的抑制功能

Cutting edge: inhibitory functions of the killer cell lectin-like receptor G1 molecule during the activation of mouse NK cells.

作者信息

Robbins Scott H, Nguyen Khuong B, Takahashi Nobuaki, Mikayama Toshifumi, Biron Christine A, Brossay Laurent

机构信息

Department of Molecular Microbiology and Immunology and Graduate Program in Pathobiology, Division of Biology and Medicine, Brown University, Providence, RI 02912. Gemini Science, San Diego, CA 92121.

出版信息

J Immunol. 2002 Mar 15;168(6):2585-9. doi: 10.4049/jimmunol.168.6.2585.

Abstract

The killer cell lectin-like receptor G1 (KLRG1) is the mouse homolog of the rat mast cell function-associated Ag and contains an immunoreceptor tyrosine-based inhibitory motif in its cytoplasmic domain. In this study we demonstrate that both pathogenic and nonpathogenic in vivo activation of NK cells induces the expression of KLRG1 on their cell surface. Upon infection with murine CMV, this induction peaks between days 5 and 7 with about 90% of the NK cells expressing KLRG1. On day 1.5 post-murine CMV infection of C57BL/6 mice, the main producers of IFN-gamma are the KLRG1-negative NK cells. This effect has been recapitulated in vitro as we show that engagement of KLRG1 on a transfected NK cell line inhibits both cytokine production and NK cell-mediated cytotoxicity. Taken together, these data illustrate the crucial role played by KLRG1 during the termination of mouse NK cell activation.

摘要

杀伤细胞凝集素样受体G1(KLRG1)是大鼠肥大细胞功能相关抗原的小鼠同源物,其胞质结构域含有基于免疫受体酪氨酸的抑制基序。在本研究中,我们证明,NK细胞在体内的致病性和非致病性激活均可诱导其细胞表面KLRG1的表达。感染鼠巨细胞病毒后,这种诱导在第5天至第7天达到峰值,约90%的NK细胞表达KLRG1。在C57BL/6小鼠感染鼠巨细胞病毒后1.5天,主要产生γ干扰素的是KLRG1阴性的NK细胞。我们在体外再现了这种效应,因为我们表明,转染的NK细胞系上KLRG1的结合可抑制细胞因子产生和NK细胞介导的细胞毒性。综上所述,这些数据说明了KLRG1在小鼠NK细胞激活终止过程中所起的关键作用。

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