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• W1005468862 abstract "Abstract Initial events after exposure determine HIV-1 disease progression, underscoring a critical need to understand host mechanisms that interfere with initial viral replication. Although associated with chronic HIV-1 control, it is not known whether interleukin-21 (IL-21) contributes to early HIV-1 immunity. Here we take advantage of tractable primary human lymphoid organ aggregate cultures to show that IL-21 directly suppresses HIV-1 replication, and identify microRNA-29 (miR-29) as an antiviral factor induced by IL-21 in CD4 T cells. IL-21 promotes transcription of all miR-29 species through STAT3, whose binding to putative regulatory regions within the MIR29 gene is enriched by IL-21 signalling. Notably, exogenous IL-21 limits early HIV-1 infection in humanized mice, and lower viremia in vivo is associated with higher miR-29 expression. Together, these findings reveal a novel antiviral IL-21-miR-29 axis that promotes CD4 T-cell-intrinsic resistance to HIV-1 infection, and suggest a role for IL-21 in initial HIV-1 control in vivo ." @default.
• W1005468862 created "2016-06-24" @default.
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• W1005468862 date "2015-06-25" @default.
• W1005468862 modified "2023-10-05" @default.
• W1005468862 title "IL-21 induces antiviral microRNA-29 in CD4 T cells to limit HIV-1 infection" @default.
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• W1005468862 doi "https://doi.org/10.1038/ncomms8562" @default.
• W1005468862 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4481879" @default.
• W1005468862 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26108174" @default.
• W1005468862 hasPublicationYear "2015" @default.
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