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

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 C. Borges, Dario S. Zamboni, Foo Y. Liew, Fernando Q. Cunha and Jose C. Alves-Filho ()
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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
Fernando Q. Cunha: Ribeirao Preto Medical School, University of Sao Paulo
Jose C. Alves-Filho: Ribeirao Preto Medical School, University of Sao Paulo

Nature Communications, 2017, vol. 8, issue 1, 1-14

Abstract: 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.

Date: 2017
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DOI: 10.1038/ncomms14919

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