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Immunity. 2015 Jun 16;42(6):1005-19. doi: 10.1016/j.immuni.2015.06.006.

Interleukin-33 in Tissue Homeostasis, Injury, and Inflammation.

Author information

1
Department of Microbiology & Immunology, University of California, San Francisco, 94143-0795, USA; Department of Laboratory Medicine, University of California, San Francisco, 94143-0795, USA.
2
Howard Hughes Medical Institute, University of California, San Francisco, 94143-0795, USA; Department of Microbiology & Immunology, University of California, San Francisco, 94143-0795, USA.
3
Howard Hughes Medical Institute, University of California, San Francisco, 94143-0795, USA; Department of Medicine, University of California, San Francisco, 94143-0795, USA; Department of Microbiology & Immunology, University of California, San Francisco, 94143-0795, USA. Electronic address: locksley@medicine.ucsf.edu.

Abstract

Interleukin-33 (IL-33) is a nuclear-associated cytokine of the IL-1 family originally described as a potent inducer of allergic type 2 immunity. IL-33 signals via the receptor ST2, which is highly expressed on group 2 innate lymphoid cells (ILC2s) and T helper 2 (Th2) cells, thus underpinning its association with helminth infection and allergic pathology. Recent studies have revealed ST2 expression on subsets of regulatory T cells, and for a role for IL-33 in tissue homeostasis and repair that suggests previously unrecognized interactions within these cellular networks. IL-33 can participate in pathologic fibrotic reactions, or, in the setting of microbial invasion, can cooperate with inflammatory cytokines to promote responses by cytotoxic NK cells, Th1 cells, and CD8(+) T cells. Here, we highlight the regulation and function of IL-33 and ST2 and review their roles in homeostasis, damage, and inflammation, suggesting a conceptual framework for future studies.

PMID:
26084021
PMCID:
PMC4471869
DOI:
10.1016/j.immuni.2015.06.006
[Indexed for MEDLINE]
Free PMC Article

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