IL-3 receptor signalling suppresses chronic intestinal inflammation by controlling mechanobiology and tissue egress of regulatory T cells.

IL-3 has been reported to be involved in various inflammatory disorders, but its role in inflammatory bowel disease (IBD) has not been addressed so far. Here, we determined IL-3 expression in samples from patients with IBD and studied the impact of or deficiency on T cell-dependent experimental colitis. We explored the mechanical, cytoskeletal and migratory properties of and T cells using real-time deformability cytometry, atomic force microscopy, scanning electron microscopy, fluorescence recovery after photobleaching and and cell trafficking assays.

Author Correction: Hobit- and Blimp-1-driven CD4 tissue-resident memory T cells control chronic intestinal inflammation.

In the version of this article initially published, a portion of the Acknowledgements section ("the Clinical Research Group CEDER of the German Research Council (DFG)") was incorrect. The correct statement is as follows: "..

Hobit- and Blimp-1-driven CD4 tissue-resident memory T cells control chronic intestinal inflammation.

Although tissue-resident memory T cells (T cells) have been shown to regulate host protection in infectious disorders, their function in inflammatory bowel disease (IBD) remains to be investigated. Here we characterized T cells in human IBD and in experimental models of intestinal inflammation. Pro-inflammatory T cells accumulated in the mucosa of patients with IBD, and the presence of CD4CD69CD103 T cells was predictive of the development of flares.