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γδ T细胞诱导的一氧化氮生成增强对黏膜念珠菌病的抵抗力。

Gamma delta T cell-induced nitric oxide production enhances resistance to mucosal candidiasis.

作者信息

Jones-Carson J, Vazquez-Torres A, van der Heyde H C, Warner T, Wagner R D, Balish E

机构信息

Department of Surgery, University of Wisconsin Medical School, Madison 53706-1532, USA.

出版信息

Nat Med. 1995 Jun;1(6):552-7. doi: 10.1038/nm0695-552.

Abstract

Despite the prevalence of gamma delta T cells in mucosae that are typically colonized by Candida albicans, little is known of the possible role of these cells in resistance to candidiasis. A sharp increase in the number of gamma delta T cells and macrophages following intraperitoneal inoculation of mice with C. albicans led us to examine the role of these cells in the immune response to C. albicans. We show that the gamma delta T cells enhance macrophage nitric oxide (NO) production and anti-candida activity, in vitro. We also propose that the gamma delta T cells regulate macrophage function during candidiasis in vivo as well, because depletion of these cells abrogated inducible NO synthase expression in mucosae and enhanced murine susceptibility to candidiasis.

摘要

尽管γδT细胞在通常被白色念珠菌定殖的黏膜中普遍存在,但对于这些细胞在抵抗念珠菌病中可能发挥的作用却知之甚少。在用白色念珠菌对小鼠进行腹腔接种后,γδT细胞和巨噬细胞的数量急剧增加,这促使我们研究这些细胞在针对白色念珠菌的免疫反应中的作用。我们发现,γδT细胞在体外可增强巨噬细胞一氧化氮(NO)的产生及抗念珠菌活性。我们还提出,γδT细胞在体内念珠菌病期间也调节巨噬细胞功能,因为去除这些细胞会消除黏膜中诱导型NO合酶的表达,并增强小鼠对念珠菌病的易感性。

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