IL-17 signaling in host defense against Candida albicans

被引:94
作者
Gaffen, Sarah L. [1 ]
Hernandez-Santos, Nydiaris [1 ]
Peterson, Alanna C. [1 ]
机构
[1] Univ Pittsburgh, Div Clin Immunol & Rheumatol, Dept Med, Pittsburgh, PA 15216 USA
基金
美国国家卫生研究院;
关键词
IL-17; Th17; Candida albicans; Fungal infections; Cytokine; HYPER-IGE SYNDROME; CHRONIC MUCOCUTANEOUS CANDIDIASIS; TH17; CELLS; T-CELLS; FUNGAL-INFECTIONS; OROPHARYNGEAL CANDIDIASIS; TH17-ASSOCIATED CYTOKINES; IL-17-PRODUCING CELLS; NLRP3; INFLAMMASOME; ADAPTIVE IMMUNITY;
D O I
10.1007/s12026-011-8226-x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The discovery of the Th17 lineage in 2005 triggered a major change in how immunity to infectious diseases is viewed. Fungal infections, in particular, have long been a relatively understudied area of investigation in terms of the host immune response. Candida albicans is a commensal yeast that colonizes mucosal sites and skin. In healthy individuals, it is non-pathogenic, but in conditions of immune deficiency, this organism can cause a variety of infections associated with considerable morbidity. Candida can also cause disseminated infections that have a high mortality rate and are a major clinical problem in hospital settings. Although immunity to Candida albicans was long considered to be mediated by Th1 cells, new data in both rodent models and in humans have revealed an essential role for the Th17 lineage, and in particular its signature cytokine IL-17.
引用
收藏
页码:181 / 187
页数:7
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