IL-17-Mediated Immunity to the Opportunistic Fungal Pathogen Candida albicans

被引:205
|
作者
Conti, Heather R. [1 ]
Gaffen, Sarah L. [1 ]
机构
[1] Univ Pittsburgh, Dept Med, Div Clin Immunol & Rheumatol, Pittsburgh, PA 15261 USA
来源
JOURNAL OF IMMUNOLOGY | 2015年 / 195卷 / 03期
基金
美国国家卫生研究院;
关键词
CHRONIC MUCOCUTANEOUS CANDIDIASIS; TUMOR-NECROSIS-FACTOR; INNATE LYMPHOID-CELLS; HOST-DEFENSE; TH17; CELLS; T-CELLS; PROTECTIVE IMMUNITY; STAT1; MUTATIONS; HUMAN DECTIN-1; IL-17; PATHWAY;
D O I
10.4049/jimmunol.1500909
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
IL-17 (IL-17A) has emerged as a key mediator of protection against extracellular microbes, but this cytokine also drives pathology in various autoimmune diseases. Overwhelming data in both humans and mice reveal a clear and surprisingly specific role for IL-17 in protection against the fungus Candida albicans, a commensal microbe of the human oral cavity, gastrointestinal tract, and reproductive mucosa. The IL-17 pathway regulates antifungal immunity through upregulation of proinflammatory cytokines, including IL-6, neutrophilrecruiting chemokines (e.g., CXCL1 and CXCL5), and antimicrobial peptides (e.g., defensins), which act in concert to limit fungal overgrowth. This review focuses on diseases caused by C. albicans, the role of IL-17-mediated immunity in candidiasis, and the implications for clinical therapies for both autoimmune conditions and fungal infections.
引用
收藏
页码:780 / 788
页数:9
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