Journal
ELIFE
Volume 5, Issue -, Pages -Publisher
ELIFE SCIENCES PUBLICATIONS LTD
DOI: 10.7554/eLife.10066
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Funding
- Wellcome Trust [095688/Z/11/Z]
- University Of Oxford NDM Studentship
- Cancer Research Institute
- Medical Research Council
- Crohn's and Colitis Foundation of America
- Crohn's and Colitis UK
- Leona M. and Harry B. Helmsley Charitable Trust
- ForCrohns
- Wellcome Trust [095688/Z/11/Z] Funding Source: Wellcome Trust
- BBSRC [BB/I005609/1] Funding Source: UKRI
- MRC [MR/L022699/1, MC_PC_13055] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/I005609/1] Funding Source: researchfish
- Medical Research Council [MC_PC_13055, MR/L022699/1] Funding Source: researchfish
- Versus Arthritis [20834] Funding Source: researchfish
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Innate lymphoid cells (ILCs) contribute to host defence and tissue repair but can induce immunopathology. Recent work has revealed tissue-specific roles for ILCs; however, the question of how a small population has large effects on immune homeostasis remains unclear. We identify two mechanisms that ILC3s utilise to exert their effects within intestinal tissue. ILC-driven colitis depends on production of granulocyte macrophage-colony stimulating factor (GM-CSF), which recruits and maintains intestinal inflammatory monocytes. ILCs present in the intestine also enter and exit cryptopatches in a highly dynamic process. During colitis, ILC3s mobilize from cryptopatches, a process that can be inhibited by blocking GM-CSF, and mobilization precedes inflammatory foci elsewhere in the tissue. Together these data identify the IL-23R/GM-CSF axis within ILC3 as a key control point in the accumulation of innate effector cells in the intestine and in the spatio-temporal dynamics of ILCs in the intestinal inflammatory response.
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