Disruption of immune regulation by microbial pathogens and resulting chronic inflammation

被引:43
作者
Barth, Kenneth [1 ]
Remick, Daniel G. [2 ]
Genco, Caroline A. [1 ]
机构
[1] Boston Univ, Sch Med, Dept Med, Infect Dis Sect, Boston, MA 02118 USA
[2] Boston Univ, Sch Med, Dept Pathol & Lab Med, Boston, MA 02118 USA
基金
美国国家卫生研究院;
关键词
NITRIC-OXIDE SYNTHASE; MYCOBACTERIUM-TUBERCULOSIS LIPOARABINOMANNAN; METHIONINE SULFOXIDE REDUCTASES; PORPHYROMONAS-GINGIVALIS; COMPLEMENT RECEPTOR-3; ANTIGEN PRESENTATION; INNATE IMMUNITY; PHOSPHATIDYLINOSITOL; 3-KINASE; TREHALOSE 6,6'-DIMYCOLATE; PHAGOSOME MATURATION;
D O I
10.1002/jcp.24299
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Activation of the immune response is a tightly regulated, coordinated effort that functions to control and eradicate exogenous microorganisms, while also responding to endogenous ligands. Determining the proper balance of inflammation is essential, as chronic inflammation leads to a wide array of host pathologies. Bacterial pathogens can instigate chronic inflammation via an extensive repertoire of evolved evasion strategies that perturb immune regulation. In this review, we discuss two model pathogens, Mycobacterium tuberculosis and Porphyromonas gingivalis, which efficiently escape various aspects of the immune system within professional and non-professional immune cell types to establish chronic inflammation. J. Cell. Physiol. 228: 14131422, 2013. (c) 2012 Wiley Periodicals, Inc.
引用
收藏
页码:1413 / 1422
页数:10
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