IL-17 and Th17 cells in tuberculosis

被引:260
|
作者
Torrado, Egidio [1 ]
Cooper, Andrea M. [1 ]
机构
[1] Trudeau Inst Inc, Saranac Lake, NY 12983 USA
关键词
Tuberculosis; Lung; Cytokines; Inflammation; Immunopathology; REGULATORY T-CELLS; MYCOBACTERIUM-TUBERCULOSIS; IMMUNE-RESPONSE; ADAPTIVE IMMUNITY; DENDRITIC CELLS; HOST-DEFENSE; INTERLEUKIN-17; PRODUCTION; KLEBSIELLA-PNEUMONIAE; ACQUIRED-IMMUNITY; TGF-BETA;
D O I
10.1016/j.cytogfr.2010.10.004
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Tuberculosis is primarily a disease of the lung. Constant expression of cellular immunity in this organ is required to control Mycobacterium tuberculosis growth, but this can also result in chronic inflammation and pathologic consequences. During primary tuberculosis both IFN-gamma and IL-17 are induced: both are potent inflammatory cytokines capable of inducing expression of chemokines that promote cell recruitment and granuloma organization throughout infection. During the chronic phase, a balance between Th1 and Th17 responses needs to be achieved to control bacterial growth and limit immunopathology, as a shift of the response towards excessive IL-17 production may sustain extensive neutrophil recruitment and tissue damage. Thus, regulation of Th1 and Th17 responses during tuberculosis is essential to promote anti-mycobacterial immunity and prevent extensive immunopathological consequences. (C) 2010 Elsevier Ltd. All rights reserved.
引用
收藏
页码:455 / 462
页数:8
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