Lipids, apoptosis, and cross-presentation: links in the chain of host defense against Mycobacterium tuberculosis

被引：56

作者：

Behar, Samuel M. ^{[1
,2
]}

Martin, Constance J. ^{[1
,2
]}

Nunes-Alves, Claudio ^{[1
]}

Divangahi, Maziar ^{[1
]}

Remold, Heinz G. ^{[1
]}

机构：

[1] Harvard Univ, Brigham & Womens Hosp, Div Rheumatol Immunol & Allergy, Sch Med,Dept Med, Boston, MA 02115 USA

[2] Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA

来源：

MICROBES AND INFECTION | 2011年 / 13卷 / 8-9期

基金：

美国国家卫生研究院;

关键词：

Microbial immunity; Tuberculosis; Infection; Eicosanoids; Cross-presentation; T cell immunity; CD8(+) T-CELLS; BACILLUS-CALMETTE-GUERIN; HUMAN DENDRITIC CELLS; IN-VIVO DEPLETION; ANTIGEN PRESENTATION; ADAPTIVE IMMUNITY; LYMPH-NODE; MACROPHAGES; INFECTION; ACTIVATION;

D O I：

10.1016/j.micinf.2011.03.002

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：

Eicosanoids regulate whether human and murine macrophages infected with Mycobacterium tuberculosis die by apoptosis or necrosis. The death modality is important since apoptosis is associated with diminished pathogen viability and should be viewed as a form of innate immunity. Apoptotic vesicles derived from infected macrophages are also an important source of bacterial antigens that can be acquired by dendritic cells to prime antigen-specific T cells. This review integrates in vitro and in vivo data on how apoptosis of infected macrophages is linked to development of T cell immunity against M. tuberculosis. (C) 2011 Institut Pasteur. Published by Elsevier Masson SAS. All rights reserved.

引用

页码：749 / 756

页数：8

共 54 条

[1]

Dendritic cells acquire antigen from apoptotic cells and induce class I restricted CTLs [J].