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. 2021 Jul 16;22(14):7618. doi: 10.3390/ijms22147618

Figure 7.

Figure 7

Influence of microbiota in other ILCs in intestinal homeostasis. (a) SCFAs produced by the commensal gut microbiota support optimal proliferation of ILC1, ILC2 and ILC3 populations by regulating G protein-coupled receptors (GPCRs). (b) In the absence of commensal bacteria, NK cells have reduced cytotoxicity and IFN-γ production. Colonization of germ-free mice with commensals increases NK cytotoxicity through the effect of dendritic cells and macrophage-derived type-I interferons on IL-15, which promotes NK cell terminal maturation. (c) LTi cells produce cryptopatches, which are transformed into isolated lymphoid follicles in a microbiota-dependent manner, supporting the production of intestinal IgA. (d) The gut microbiota enhances the expression of T-bet in ILCs. (e) The proportion of ILC2s in the gut is increased in the absence of commensal microbiota. (f) The microbiota regulates ILC2 function in the gut by promoting the release of IL-25, which drives ILC2s to improve intestinal barrier function.