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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

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

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Nascimento, Daniele C. ; Melo, Paulo H. ; Pineros, Annie R. ; Ferreira, Raphael G. ; Colon, 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.
Total Authors: 15
Document type: Journal article
Source: NATURE COMMUNICATIONS; v. 8, APR 4 2017.
Web of Science Citations: 40
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. (AU)

FAPESP's process: 13/08216-2 - CRID - Center for Research in Inflammatory Diseases
Grantee:Fernando de Queiroz Cunha
Support type: Research Grants - Research, Innovation and Dissemination Centers - RIDC
FAPESP's process: 11/19670-0 - Mechanisms involved in the pathophysiology of rheumatoid arthritis, pain and sepsis
Grantee:Fernando de Queiroz Cunha
Support type: Research Projects - Thematic Grants