期刊
CLINICAL AND TRANSLATIONAL MEDICINE
卷 6, 期 -, 页码 -出版社
SPRINGEROPEN
DOI: 10.1186/s40169-017-0151-8
关键词
Tuberculosis; Protection; Pathogenesis; IFN-gamma; CD4(+) T cell; TB-IRIS; Macrophage; Neutrophil; Necrosis; Matrix metalloproteinase; Granuloma
IFN gamma-producing CD4(+) T cells (IFN gamma(+)CD4(+) T cells) are the key orchestrators of protective immunity against Mycobacterium tuberculosis (Mtb). Primarily, these cells act by enabling Mtb-infected macrophages to enforce phagosome-lysosome fusion, produce reactive nitrogen intermediates (RNIs), and activate autophagy pathways. However, TB is a heterogeneous disease and a host of clinical and experimental findings has also implicated IFN gamma+CD4(+) T cells in TB pathogenesis. High frequency of IFN gamma(+) CD4(+) T cells is the most invariable feature of the active disease. Active TB patients mount a heightened IFN gamma(+) CD4(+) T cell response to mycobacterial antigens and demonstrate an IFN gamma-inducible transcriptomic signature. IFN gamma(+) CD4(+) T cells have also been shown to mediate TB-associated immune reconstitution inflammatory syndrome (TB-IRIS) observed in a subset of antiretroviral therapy (ART)-treated HIV- and Mtb-coinfected people. The pathological face of IFN gamma(+) CD4(+) T cells during mycobacterial infection is further uncovered by studies in the animal model of TB-IRIS and in Mtb-infected PD-1(-/-) mice. This manuscript encompasses the evidence supporting the dual role of IFN gamma(+) CD4(+) T cells during Mtb infection and sheds light on immune mechanisms involved in protection versus pathogenesis.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据