Early immune senescence in HIV disease

被引：180

作者：

Desai S. ^{[1
]}

Landay A. ^{[1
]}

机构：

[1] Department of Immunology/Microbiology, Rush University Medical Center, Chicago, IL 60612

来源：

Current HIV/AIDS Reports | 2010年 / 7卷 / 1期

关键词：

Activation; Inflammation; Microbial translocation; Senescene;

D O I：

10.1007/s11904-009-0038-4

中图分类号：

学科分类号：

摘要：

Non-AIDS-defining co-morbidities that occur despite viral suppression and immune reconstitution using antiretroviral therapy depict early aging process in HIV-infected individuals. During aging, a reduction in T-cell renewal, together with a progressive enrichment of terminally differentiated T cells, translates into a general decline of the immune system, gradually leading to immunosenescence. Inflammation is a hallmark of age-associated comorbidities, and immune activation is a hallmark of HIV disease. Constant stimulation of the immune system by HIV or due to co-infections activates the innate and adaptive immune system, resulting in release of mediators of inflammation. Immune activation coupled with lack of anti-inflammatory responses likely results in accelerated aging in HIV disease. Dysfunctional thymic output, along with HIV-mediated disruption of the gastrointestinal barrier leading to microbial translocation, contributes to the circulating antigenic load driving early senescence in HIV disease. © 2010 Springer Science+Business Media, LLC.

引用

页码：4 / 10

页数：6

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