Fig. 2: T-ILC2 interactions in response to parasite infection and allergen exposure.
From: The interplay between innate lymphoid cells and T cells
a Allergen exposure induces the release of IL-33 by lung epithelial cells, which in turn stimulates IL-13 production by tissue-resident ILC2s. ILC2-derived IL-13 promotes the activation of dendritic cells (DC) as well as their migration towards the draining lymph nodes where naïve T cells are activated and converted into Th2 cells. Th2 cells eventually migrate back to the tissue in response to DC-derived CCL17128 (b). T-ILC2 interactions also take place in the lungs and promote adaptive immune responses: antigen presentation through MHCII and OX40-OX40L interactions favors Th2 differentiation and the maintenance of memory T cells.148 c Upon helminthes infection, a specialized subset of intestinal epithelial cells named Tuft cells release IL-25. IL-25 induces the activation of inflammatory ILC2s and their exit into the blood. Circulating inflammatory ILC2s reach the lung where they can promote parasite clearance through the release of IL-13 and the activation and mucus production by goblet cells.79 T-ILC interactions such as antigen presentation, OX40–OX40L125 binding and IL-2 production75,119 coordinate innate and adaptive immunity in the small intestine to promote parasite expulsion.
