先天免疫系统
免疫系统
生物
细胞生物学
免疫学
先天性淋巴细胞
获得性免疫系统
缺氧诱导因子
调节器
CCL18型
生物化学
基因
作者
Victor Nizet,Randall S. Johnson
出处
期刊:Nature Reviews Immunology
[Springer Nature]
日期:2009-09-01
卷期号:9 (9): 609-617
被引量:626
摘要
At low levels of oxygen at sites of tissue infection, innate immune cells can adapt to survive and even enhance their antimicrobial functions. Recent studies show how this is controlled by hypoxia-inducible factor (HIF) downstream of nuclear factor-κB activation. Hypoxia-inducible factor (HIF) is an important transcriptional regulator of cell metabolism and the adaptation to cellular stress caused by oxygen deficiency (hypoxia). Phagocytic cells have an essential role in innate immune defence against pathogens and this is a battle that takes place mainly in the hypoxic microenvironments of infected tissues. It has now become clear that HIF promotes the bactericidal activities of phagocytic cells and supports the innate immune functions of dendritic cells, mast cells and epithelial cells. In response to microbial pathogens, HIF expression is upregulated through pathways involving the key immune response regulator nuclear factor-κB, highlighting an interdependence of the innate immune and hypoxic responses to infection and tissue damage. In turn, HIF-driven innate immune responses have important consequences for both the pathogen and the host, such that the tissue microenvironment fundamentally influences susceptibility to infectious disease.
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