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Innate immune recognition of infected apoptotic cells directs TH17 cell differentiation

Author

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  • Miriam Beer Torchinsky

    (Immunology Institute, Mount Sinai School of Medicine, 1425 Madison Avenue, New York, New York 10029, USA)

  • Johan Garaude

    (Immunology Institute, Mount Sinai School of Medicine, 1425 Madison Avenue, New York, New York 10029, USA)

  • Andrea P. Martin

    (Immunology Institute, Mount Sinai School of Medicine, 1425 Madison Avenue, New York, New York 10029, USA)

  • J. Magarian Blander

    (Immunology Institute, Mount Sinai School of Medicine, 1425 Madison Avenue, New York, New York 10029, USA)

Abstract

Innate immunity and apoptosis This paper identifies the apoptotic cell engulfment of infected cells as a prominent signal for the induction of TH17 cells, the subset of interleukin 17-producing T helper cells thought to be involved in autoimmunity. This demonstrates that infected apoptotic cells are a critical component of the innate immune signals instructing TH17 differentiation, and point to pathogens particularly adept at triggering apoptosis that might preferentially induce TH17-mediated immunity. Investigation of the pathways of innate recognition of infected apoptotic cells might lead to improved understanding of the causative defects in autoimmunity.

Suggested Citation

  • Miriam Beer Torchinsky & Johan Garaude & Andrea P. Martin & J. Magarian Blander, 2009. "Innate immune recognition of infected apoptotic cells directs TH17 cell differentiation," Nature, Nature, vol. 458(7234), pages 78-82, March.
    • Handle: RePEc:nat:nature:v:458:y:2009:i:7234:d:10.1038_nature07781
    DOI: 10.1038/nature07781
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    Cited by:

    1. Amir Kumar Singh & Ritesh Kumar & Jianyi Yin & John F. Brooks II & Mahesh Kathania & Sandip Mukherjee & Jitendra Kumar & Kevin P. Conlon & Venkatesha Basrur & Zhe Chen & Xianlin Han & Lora V. Hooper &, 2023. "RORĪ³t-Raftlin1 complex regulates the pathogenicity of Th17 cells and colonic inflammation," Nature Communications, Nature, vol. 14(1), pages 1-15, December.

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