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来自gp49B基因敲除突变小鼠的自然杀伤细胞和肥大细胞具有功能。

Natural killer cells and mast cells from gp49B null mutant mice are functional.

作者信息

Rojo S, Stebbins C C, Peterson M E, Dombrowicz D, Wagtmann N, Long E O

机构信息

Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland 20852, USA.

出版信息

Mol Cell Biol. 2000 Oct;20(19):7178-82. doi: 10.1128/MCB.20.19.7178-7182.2000.

Abstract

Immune responses are controlled by a combination of positive and negative cellular signals. Effector cells in the immune system express inhibitory receptors that serve to limit effector cell expansion and to protect the host from autoreactivity. gp49B is a receptor of unknown function that is expressed on activated mast cells and natural killer (NK) cells and whose cytoplasmic tail endows it with inhibitory potential. To gain insight into the function of gp49B in mice, we disrupted the gp49B gene by homologous recombination. gp49B(0) mice were born at expected ratios, were healthy and fertile, and displayed normal long-term survival rates. gp49B(0) mice showed no defect in NK or mast cell development. Furthermore, NK and mast cells from the gp49B(0) mice showed activation properties in vitro similar to those of cells isolated from wild-type mice. Therefore, gp49B is not critical for the development, expansion, and maturation of mast cells and NK cells in vivo. The healthy status of gp49B(0) mice makes them suitable for testing the role of gp49B in immune responses to infectious agents.

摘要

免疫反应由正负细胞信号共同控制。免疫系统中的效应细胞表达抑制性受体,这些受体可限制效应细胞的扩增,并保护宿主免受自身反应性的影响。gp49B是一种功能未知的受体,在活化的肥大细胞和自然杀伤(NK)细胞上表达,其细胞质尾部赋予它抑制潜能。为了深入了解gp49B在小鼠中的功能,我们通过同源重组破坏了gp49B基因。gp49B(0)小鼠以预期比例出生,健康且可育,并表现出正常的长期存活率。gp49B(0)小鼠在NK或肥大细胞发育方面没有缺陷。此外,来自gp49B(0)小鼠的NK细胞和肥大细胞在体外表现出与从野生型小鼠分离的细胞相似的活化特性。因此,gp49B对体内肥大细胞和NK细胞的发育、扩增和成熟并不关键。gp49B(0)小鼠的健康状态使其适合用于测试gp49B在对感染因子的免疫反应中的作用。

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本文引用的文献

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J Immunol. 2000 May 15;164(10):5215-20. doi: 10.4049/jimmunol.164.10.5215.
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