TY - JOUR TI - ILC3 GM-CSF production and mobilisation orchestrate acute intestinal inflammation AU - Pearson, Claire AU - Thornton, Emily E AU - McKenzie, Brent AU - Schaupp, Anna-Lena AU - Huskens, Nicky AU - Griseri, Thibault AU - West, Nathaniel AU - Tung, Sim AU - Seddon, Benedict P AU - Uhlig, Holm H AU - Powrie, Fiona A2 - Rath, Satyajit VL - 5 PY - 2016 DA - 2016/01/18 SP - e10066 C1 - eLife 2016;5:e10066 DO - 10.7554/eLife.10066 UR - https://doi.org/10.7554/eLife.10066 AB - 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. KW - live imaging KW - innate lymphoid cell KW - mucosal immunology KW - colitis JF - eLife SN - 2050-084X PB - eLife Sciences Publications, Ltd ER -