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Updated: May 29, 2026

Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice

Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4⁺CD45RB^high T Cells into Immunodeficient Mice

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Interleukin 37 expression protects mice from colitis.

Eóin N McNamee¹, Joanne C Masterson, Paul Jedlicka

¹Department of Medicine, Section of Pediatric Gastroenterology, Digestive Health Institute, Children's Hospital Colorado, University of Colorado Denver, Aurora, CO 80045, USA.

Proceedings of the National Academy of Sciences of the United States of America

|August 30, 2011

Summary

This summary is machine-generated.

Interleukin-37 (IL-37) significantly reduces experimental colitis severity in mice. This innate immunity inhibitor, when expressed in transgenic mice, lowers inflammation and protects the colon, highlighting its therapeutic potential.

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Published on: December 16, 2021

Area of Science:

Immunology
Gastroenterology
Molecular Biology

Background:

Interleukin-37 (IL-37) is a newly identified member of the IL-1 family known for inhibiting innate inflammation.
The role of IL-37 in intestinal inflammation, specifically experimental colitis, has not been fully elucidated.

Purpose of the Study:

To investigate the therapeutic potential of IL-37 in dextran sulfate sodium (DSS)-induced experimental colitis.
To determine the mechanisms underlying IL-37's anti-inflammatory effects in the colon.

Main Methods:

Generation of a transgenic mouse strain expressing human IL-37 (hIL-37tg).
Induction of colitis using DSS in hIL-37tg and wild-type (WT) mice.
Assessment of clinical and histological disease scores, leukocyte recruitment, and cytokine release (IL-1β, TNFα, IL-10).
Bone marrow transplantation experiments to investigate the cellular origin of IL-37's effects.

Main Results:

IL-37 expression in the colon increased significantly during DSS-induced colitis in hIL-37tg mice.
hIL-37tg mice exhibited reduced clinical disease scores and histological damage compared to WT mice.
Reduced leukocyte infiltration, decreased IL-1β and TNFα release, and increased IL-10 release were observed in hIL-37tg mice.
IL-37's anti-inflammatory effects were independent of IL-10 signaling and sufficient when originating from hematopoietic cells.

Conclusions:

IL-37 acts as a potent endogenous inhibitor of innate inflammation in the context of experimental colitis.
IL-37 demonstrates significant protective effects against DSS-induced colitis, reducing inflammation and tissue damage.
Hematopoietic cells are a key source of IL-37 mediating its protective role in intestinal inflammation.