ILC3 GM-CSF production and mobilisation orchestrate acute intestinal inflammation
AuthorPearson, C; Thornton, EE; McKenzie, B; Schaupp, A-L; Huskens, N; Griseri, T; West, N; Tung, S; Seddon, BP; Uhlig, HH; ...
PublisherELIFE SCIENCES PUBLICATIONS LTD
University of Melbourne Author/sMcKenzie, Brent
Document TypeJournal Article
CitationsPearson, C., Thornton, E. E., McKenzie, B., Schaupp, A. -L., Huskens, N., Griseri, T., West, N., Tung, S., Seddon, B. P., Uhlig, H. H. & Powrie, F. (2016). ILC3 GM-CSF production and mobilisation orchestrate acute intestinal inflammation. ELIFE, 5 (JANUARY2016), https://doi.org/10.7554/eLife.10066.
Access StatusOpen Access
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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