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PLoS One. 2008 Apr 2;3(4):e1915. doi: 10.1371/journal.pone.0001915.

Toll-like receptor ligands induce human T cell activation and death, a model for HIV pathogenesis.

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  • 1Department of Molecular Biology and Microbiology, Case Western Reserve University, Cleveland, Ohio, United States of America.



Recently, heightened systemic translocation of microbial products was found in persons with chronic HIV infection and this was linked to immune activation and CD4(+) T cell homeostasis.


We examined here the effects of microbial Toll-like receptor (TLR) ligands on T cell activation in vitro.


We show that exposure to TLR ligands results in activation of memory and effector CD4(+) and CD8(+) T cells. After exposure to each of 8 different ligands that activate TLRs 2, 3, 4, 5, 7, 8, and 9, CD8(+) T cells are activated and gain expression of the C type lectin CD69 that may promote their retention in lymphoid tissues. In contrast, CD4(+) T cells rarely increase CD69 expression but instead enter cell cycle. Despite activation and cell cycle entry, CD4(+) T cells divide poorly and instead, disproportionately undergo activation-induced cell death. Systemic exposure to TLR agonists may therefore increase immune activation, effector cell sequestration in lymphoid tissues and T cell turnover. These events may contribute to the pathogenesis of immune dysfunction and CD4+ T cell losses in chronic infection with the human immunodeficiency virus.

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