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Eur J Immunol. 2016 May;46(5):1067-81. doi: 10.1002/eji.201545828.

Suppression of innate inflammation and immunity by interleukin-37.

Author information

1
University of Colorado Denver, Aurora, CO, USA.
2
Radboud University Medical Center, Nijmegen, The Netherlands.
3
Monash University, Melbourne, Australia.
4
Konkuk University, Seoul, Republic of Korea.
5
Ludwig-Maximilian-University, Munich, Germany.

Abstract

IL-37 is unique in the IL-1 family in that unlike other members of the family, IL-37 broadly suppresses innate immunity. IL-37 can be elevated in humans with inflammatory and autoimmune diseases where it likely functions to limit inflammation. Transgenic mice expressing human IL-37 (IL37-tg) exhibit less severe inflammation in models of endotoxin shock, colitis, myocardial infarction, lung, and spinal cord injury. IL37-tg mice have reduced antigen-specific responses and dendritic cells (DCs) from these mice exhibit characteristics of tolerogenic DCs. Compared to aging wild-type (WT) mice, aging IL37-tg mice are protected against B-cell leukemogenesis and heart failure. Treatment of WT mice with recombinant human IL-37 has been shown to be protective in several models of inflammation and injury. IL-37 binds to the IL-18 receptor but then recruits the orphan IL-1R8 (formerly TIR8 or SIGIRR) in order to function as an inhibitor. Here, we review the discovery of IL-37, its production, release, and mechanisms by which IL-37 reduces inflammation and suppresses immune responses. The data reviewed here suggest a therapeutic potential for IL-37.

KEYWORDS:

Autoinflammation; Caspase-1; IL-1 family; Toll receptors

PMID:
27060871
PMCID:
PMC5003108
DOI:
10.1002/eji.201545828
[Indexed for MEDLINE]
Free PMC Article

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