IL-23–responsive innate lymphoid cells are increased in inflammatory bowel disease

By A. Geremia, C. Arancibia-Cárcamo, M. Fleming, N. Rust, Baljit Singh, N. Mortensen, S. Travis, F. Powrie. Journal of Experimental Medicine, 2011

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Increased numbers of innate lymphoid cells in patients with inflammatory bowel disease.

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Intraepithelial type 1 innate lymphoid cells are a unique subset of cytokine responsive interferon-γ-producing cells (2013, positive): “During IBD, dysregulated T cell production of IFN-g and IL-17 causes excessive inflammation, tissue damage, and loss of barrier function (Geremia et al., 2011; Strober and Fuss, 2011).”
Cytokine Networks in the Pathophysiology of Inflammatory Bowel Disease. (2019, background): “which are found in increased abundance in the intestine of IBD patients (Fuchs et al., 2013; Geremia et al., 2011), can contribute to the production of colitogenic effector cytokines”
The Aryl Hydrocarbon Receptor Regulates Gut Immunity through Modulation of Innate Lymphoid Cells (2011, background): “IL-23 signaling is important for the function of ILCs during colitis inmice and in humans (Buonocore et al., 2010; Geremia et al., 2011), presumably when large amounts of IL-23 are produced by antigen-presenting cells because of activation of pattern recognition receptors.”
Innate and adaptive immunity in inflammatory bowel disease. (2014, result): “In accordance with these findings, we have observed a marked and selective increase in IL-17A-producing CD56− ILCs in the inflamed intestine of patients with CD [53].”