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IL-33 contributes to sepsis-induced long-term immunosuppression by expanding the regulatory T cell population

Author

Listed:
  • Daniele C. Nascimento

    (Ribeirao Preto Medical School, University of Sao Paulo)

  • Paulo H. Melo

    (Ribeirao Preto Medical School, University of Sao Paulo)

  • Annie R. Piñeros

    (Ribeirao Preto Medical School, University of Sao Paulo)

  • Raphael G. Ferreira

    (Ribeirao Preto Medical School, University of Sao Paulo)

  • David F. Colón

    (Ribeirao Preto Medical School, University of Sao Paulo)

  • Paula B. Donate

    (Ribeirao Preto Medical School, University of Sao Paulo)

  • Fernanda V. Castanheira

    (Ribeirao Preto Medical School, University of Sao Paulo)

  • Aline Gozzi

    (Ribeirao Preto Medical School, University of Sao Paulo)

  • Paula G. Czaikoski

    (Ribeirao Preto Medical School, University of Sao Paulo)

  • Wanda Niedbala

    (Institute of Infection, Immunity and Inflammation, University of Glasgow)

  • Marcos C. Borges

    (Ribeirao Preto Medical School, University of Sao Paulo)

  • Dario S. Zamboni

    (Ribeirao Preto Medical School, University of Sao Paulo)

  • Foo Y. Liew

    (Institute of Infection, Immunity and Inflammation, University of Glasgow
    School of Biology and Basic Medical Sciences, Soochow University)

  • Fernando Q. Cunha

    (Ribeirao Preto Medical School, University of Sao Paulo)

  • Jose C. Alves-Filho

    (Ribeirao Preto Medical School, University of Sao Paulo)

Abstract

Patients who survive sepsis can develop long-term immune dysfunction, with expansion of the regulatory T (Treg) cell population. However, how Treg cells proliferate in these patients is not clear. Here we show that IL-33 has a major function in the induction of this immunosuppression. Mice deficient in ST2 (IL-33R) develop attenuated immunosuppression in cases that survive sepsis, whereas treatment of naive wild-type mice with IL-33 induces immunosuppression. IL-33, released during tissue injury in sepsis, activates type 2 innate lymphoid cells, which promote polarization of M2 macrophages, thereby enhancing expansion of the Treg cell population via IL-10. Moreover, sepsis-surviving patients have more Treg cells, IL-33 and IL-10 in their peripheral blood. Our study suggests that targeting IL-33 may be an effective treatment for sepsis-induced immunosuppression.

Suggested Citation

  • Daniele C. Nascimento & Paulo H. Melo & Annie R. Piñeros & Raphael G. Ferreira & David F. Colón & Paula B. Donate & Fernanda V. Castanheira & Aline Gozzi & Paula G. Czaikoski & Wanda Niedbala & Marcos, 2017. "IL-33 contributes to sepsis-induced long-term immunosuppression by expanding the regulatory T cell population," Nature Communications, Nature, vol. 8(1), pages 1-14, April.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms14919
    DOI: 10.1038/ncomms14919
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    Cited by:

    1. Juliane Glaubitz & Anika Wilden & Janine Golchert & Georg Homuth & Uwe Völker & Barbara M. Bröker & Thomas Thiele & Markus M. Lerch & Julia Mayerle & Ali A. Aghdassi & Frank U. Weiss & Matthias Sendle, 2022. "In mouse chronic pancreatitis CD25+FOXP3+ regulatory T cells control pancreatic fibrosis by suppression of the type 2 immune response," Nature Communications, Nature, vol. 13(1), pages 1-20, December.

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