IL-33 contributes to sepsis-induced long-term immunosuppression by expanding the regulatory T cell population.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 28374774.
- Also identified by DOI 10.1038/ncomms14919 and PMC identifier 5382289.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
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.
Medical subject headings
- Immune Tolerance
- Interleukin-33
- Sepsis
- T-Lymphocytes, Regulatory