IL-21 induces antiviral microRNA-29 in CD4 T cells to limit HIV-1 infection

Stanley Adoro, Juan R. Cubillos-Ruiz, Xi Chen, Maud Deruaz, Vladimir D. Vrbanac, Minkyung Song, Suna Park, Thomas T. Murooka, Timothy E. Dudek, Andrew D. Luster, Andrew M. Tager, Hendrik Streeck, Brittany Bowman, Bruce D. Walker, Douglas S. Kwon, Vanja Lazarevic and Laurie H. Glimcher ()
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Stanley Adoro: Weill Cornell Medical College, Cornell University, 1300 York Avenue, New York, New York 10065, USA
Juan R. Cubillos-Ruiz: Weill Cornell Medical College, Cornell University, 1300 York Avenue, New York, New York 10065, USA
Xi Chen: Weill Cornell Medical College, Cornell University, 1300 York Avenue, New York, New York 10065, USA
Maud Deruaz: Center for Immunology and Inflammatory Diseases, Allergy and Immunology, Massachusetts General Hospital
Vladimir D. Vrbanac: Ragon Institute of MGH, MIT and Harvard
Minkyung Song: Weill Cornell Medical College, Cornell University, 1300 York Avenue, New York, New York 10065, USA
Suna Park: Weill Cornell Medical College, Cornell University, 1300 York Avenue, New York, New York 10065, USA
Thomas T. Murooka: Center for Immunology and Inflammatory Diseases, Allergy and Immunology, Massachusetts General Hospital
Timothy E. Dudek: Ragon Institute of MGH, MIT and Harvard
Andrew D. Luster: Center for Immunology and Inflammatory Diseases, Allergy and Immunology, Massachusetts General Hospital
Andrew M. Tager: Ragon Institute of MGH, MIT and Harvard
Hendrik Streeck: Institute for Medical Biology, University Hospital Essen, University of Duisburg-Essen
Brittany Bowman: Ragon Institute of MGH, MIT and Harvard
Bruce D. Walker: Ragon Institute of MGH, MIT and Harvard
Douglas S. Kwon: Ragon Institute of MGH, MIT and Harvard
Vanja Lazarevic: Experimental Immunology Branch, National Cancer Institute, NIH
Laurie H. Glimcher: Weill Cornell Medical College, Cornell University, 1300 York Avenue, New York, New York 10065, USA

Nature Communications, 2015, vol. 6, issue 1, 1-12

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.

Date: 2015
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DOI: 10.1038/ncomms8562

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