Th17 cells in pathogenic simian immunodeficiency virus infection of macaques.
Th17 cells in pathogenic simian immunodeficiency virus infection of macaques.
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DOI：
10.1097/coh.0b013e32833653ec
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发表时间：
2010-03
影响因子：
4.1
通讯作者：
Franchini G
中科院分区：
文献类型：
--
作者：
Cecchinato V;Franchini G
We discuss studies on a subset of CD4+T-cells, designated Th17, and their role in the pathogenesis of human and simian acquired immune deficiency, caused by infection with HIV and SIV respectively. Most Th17 cells are lost within two weeks from infection at mucosal sites of SIV-infected macaques and are not replenished over time. Comparison of simian pathogenic and non pathogenic models of SIV infection suggests that Th17 cells contribute to the pathogenesis of AIDS. Th17 cells, a recently identified subset of T helper cells, play a major role in both inducing auto-immune disorders and fencing off extracellular pathogens. Several groups have reported that the number of Th17 cells is decreased in the gut of HIV and SIV infected hosts. The loss of Th17 cells from the mucosal compartment has been associated to the dissemination of Salmonella typhimurium that is normally contained locally by the host immune system. It is believed that microbial translocation sustains immune activation in HIV infection and contributes to AIDS. Understanding the mechanisms that lead to disruption of mucosal integrity, viral spread, and chronic immune activation is of crucial importance for the design of efficient vaccines and therapeutic intervention for HIV.
