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ILC3 GM-CSF Production and Mobilisation Orchestrate Acute Intestinal Inflammation

ILC3 GM-CSF Production and Mobilisation Orchestrate Acute Intestinal Inflammation

Claire Pearson, Emily E Thornton, Brent McKenzie, Anna-Lena Schaupp, Nicky Huskens, Thibault Griseri, Nathaniel West, Sim Tung, Benedict P Seddon, Holm H Uhlig, Fiona Powrie

Elife. 2016 Jan 18;5:e10066.

PMID: 26780670

Abstract:

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.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
IAR4248587	Granulocyte-Macrophage Colony-Stimulating Factor from mouse			Price

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