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- W2604332021 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." @default.
- W2604332021 created "2017-04-14" @default.
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- W2604332021 date "2017-04-01" @default.
- W2604332021 modified "2023-10-10" @default.
- W2604332021 title "IL-33 contributes to sepsis-induced long-term immunosuppression by expanding the regulatory T cell population" @default.
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- W2604332021 doi "https://doi.org/10.1038/ncomms14919" @default.
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