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

England: Nature Publishing Group

Erscheinungsjahr

2017

Link zum Volltext

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.