Details

Autor(en) / Beteiligte

• Nascimento, Daniele C.
• Melo, Paulo H.
• Piñeros, Annie R.
• Ferreira, Raphael G.
• Colón, David F.
• Donate, Paula B.
• Castanheira, Fernanda V.
• Gozzi, Aline
• Czaikoski, Paula G.
• Niedbala, Wanda
• Borges, Marcos C.
• Zamboni, Dario S.
• Liew, Foo Y.
• Cunha, Fernando Q.
• Alves-Filho, Jose C.

Titel

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

Ist Teil von

• Nature communications, 2017-04, Vol.8 (1), p.14919-14919, Article 14919

Ort / Verlag

London: Nature Publishing Group UK

Erscheinungsjahr

2017

Quelle

MEDLINE

Beschreibungen/Notizen

• 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. Patients who survive sepsis are at increased risk of infection owing to long-term immunosuppression that is associated with an increase in Treg cell numbers. Here the authors show expansion of the Treg cell population in sepsis mice is driven by IL-33-induced ILC2 activation of IL-10 production by macrophages.