Journal
NATURE IMMUNOLOGY
Volume 16, Issue 1, Pages 118-+Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.3036
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Funding
- National MS Society [CA1061-A-18]
- US National Institutes of Health [P01 AI045757, U19 AI046130, U19 AI070352, P01 AI039671, R01 AI065309]
- Penates Foundation
- Nancy Taylor Foundation for Chronic Diseases
- Race to Erase MS Foundation
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The recognition of microbial patterns by Toll-like receptors (TLRs) is critical for activation of the innate immune system. Although TLRs are expressed by human CD4(+) T cells, their function is not well understood. Here we found that engagement of TLR7 in CD4(+) T cells induced intracellular calcium flux with activation of an anergic gene-expression program dependent on the transcription factor NFATc2, as well as unresponsiveness of T cells. As chronic infection with RNA viruses such as human immunodeficiency virus type 1 (HIV-1) induces profound dysfunction of CD4(+) T cells, we investigated the role of TLR7-induced anergy in HIV-1 infection. Silencing of TLR7 markedly decreased the frequency of HIV-1-infected CD4(+) T cells and restored the responsiveness of those HIV-1(+) CD4(+) T cells. Our results elucidate a previously unknown function for microbial pattern-recognition receptors in the downregulation of immune responses.
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