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

Nascimento, D. C. et al. (2017) IL-33 contributes to sepsis-induced long-term immunosuppression by expanding the regulatory T cell population. Nature Communications, 8, 14919. (doi: 10.1038/ncomms14919) (PMID:28374774) (PMCID:PMC5382289)

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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.

Item Type:Articles
Status:Published
Refereed:Yes
Glasgow Author(s) Enlighten ID:Liew, Prof Foo and Niedbala, Dr Wanda
Authors: Nascimento, D. C., Melo, P. H., Piñeros, A. R., Ferreira, R. G., Colón, D. F., Donate, P. B., Castanheira, F. V., Gozzi, A., Czaikoski, P. G., Niedbala, W., Borges, M. C., Zamboni, D. S., Liew, F. Y., Cunha, F. Q., and Alves-Filho, J. C.
College/School:College of Medical Veterinary and Life Sciences > Institute of Infection Immunity and Inflammation
Journal Name:Nature Communications
Publisher:Nature Publishing Group
ISSN:2041-1723
ISSN (Online):2041-1723
Copyright Holders:Copyright © 2017 The Authors
First Published:First published in Nature Communications 8:14919
Publisher Policy:Reproduced under a Creative Commons License

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