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

Author

Listed:
  • Stanley Adoro

    (Weill Cornell Medical College, Cornell University, 1300 York Avenue, New York, New York 10065, USA
    Ragon Institute of MGH, MIT and Harvard)

  • Juan R. Cubillos-Ruiz

    (Weill Cornell Medical College, Cornell University, 1300 York Avenue, New York, New York 10065, USA
    Ragon Institute of MGH, MIT and Harvard)

  • 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
    Center for Immunology and Inflammatory Diseases, Allergy and Immunology, Massachusetts General Hospital)

  • 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
    Center for Immunology and Inflammatory Diseases, Allergy and Immunology, Massachusetts General Hospital)

  • 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
    Howard Hughes Medical Institute
    Chevy Chase)

  • 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
    Ragon Institute of MGH, MIT and Harvard)

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.

Suggested Citation

  • 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 St, 2015. "IL-21 induces antiviral microRNA-29 in CD4 T cells to limit HIV-1 infection," Nature Communications, Nature, vol. 6(1), pages 1-12, November.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms8562
    DOI: 10.1038/ncomms8562
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