Alveolar macrophages and type I IFN in airway homeostasis and immunity

被引:132
作者
Divangahi, Maziar [1 ,2 ]
King, Irah L. [2 ]
Pernet, Erwan [1 ]
机构
[1] McGill Univ, McGill Int TB Ctr, Dept Pathol, Meakins Christie Labs,Dep Med,Hlth Ctr, Montreal, PQ, Canada
[2] McGill Univ, Dept Microbiol & Immunol, Microbiome & Dis Tolerance Ctr, Montreal, PQ, Canada
基金
加拿大自然科学与工程研究理事会;
关键词
alveolar macrophages; host defense; pulmonary infection; tissue homeostasis; type I interferon; HEMATOPOIETIC STEM-CELLS; NF-KAPPA-B; PERSISTENT LCMV INFECTION; OXYGEN SPECIES PRODUCTION; NOD-LIKE RECEPTOR; MYCOBACTERIUM-TUBERCULOSIS; ANTIVIRAL IMMUNITY; INNATE IMMUNITY; CIRCULATING MONOCYTES; CROSS-PRESENTATION;
D O I
10.1016/j.it.2015.03.005
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
071005 [微生物学]; 100108 [医学免疫学];
摘要
Globally, respiratory infections cause more than 4 million deaths per year, with influenza and tuberculosis (TB) in particular being major causes of mortality and morbidity. Although immune cell activation is critical for killing respiratory pathogens, this response must be tightly regulated to effectively control and eliminate invading microorganisms while minimizing immunopathology and maintaining pulmonary function. The distinct microenvironment of the lung is constantly patrolled by alveolar macrophages (M phi), which are essential for tissue homeostasis, early pathogen recognition, initiation of the local immune response, and resolution of inflammation. Here, we focus on recent advances that have provided insight into the relation between pulmonary M phi, type I interferon (IFN) signaling, and the delicate balance between protective and pathological immune responses in the lung.
引用
收藏
页码:307 / 314
页数:8
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