Immune reconstitution inflammatory syndrome: the trouble with immunity when you had none

被引：125

作者：

Barber, Daniel L. ^{[1
]}

Andrade, Bruno B. ^{[1
]}

Sereti, Irini ^{[2
]}

Sher, Alan ^{[1
]}

机构：

[1] NIAID, Immunobiol Sect, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA

[2] NIAID, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA

来源：

NATURE REVIEWS MICROBIOLOGY | 2012年 / 10卷 / 02期

基金：

美国国家卫生研究院;

关键词：

PROGRESSIVE MULTIFOCAL LEUKOENCEPHALOPATHY; HIV-INFECTED PATIENTS; PNEUMOCYSTIS-CARINII-PNEUMONIA; CD4(+) T-CELLS; ANTIRETROVIRAL THERAPY; RISK-FACTORS; MYCOBACTERIUM-TUBERCULOSIS; HOMEOSTATIC PROLIFERATION; CRYPTOCOCCAL MENINGITIS; PARADOXICAL RESPONSE;

D O I：

10.1038/nrmicro2712

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

Some individuals who are infected with HIV rapidly deteriorate shortly after starting antiretroviral therapy, despite effective viral suppression. This reaction, referred to as immune reconstitution inflammatory syndrome ( IRIS), is characterized by tissue-destructive inflammation and arises as CD4(+) T cells re-emerge. It has been proposed that IRIS is caused by a dysregulation of the expanding population of CD4(+) T cells specific for a co-infecting opportunistic pathogen. Here, we argue that IRIS instead results from hyper-responsiveness of the innate immune system to T cell help, a mechanism that may be shared by the many manifestations of IRIS that occur following the reversal of other types of immunosuppression in pathogen-infected hosts.

引用

页码：150 / 156

页数：7

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