Fig. 1: Coordinated innate and adaptive immune responses to commensal bacteria in the small intestine.
From: The interplay between innate lymphoid cells and T cells
a In the small intestine, the commensal Segmented filamentous bacteria induce IL-22 production by ILC3s, which in turn promotes the local maturation of Th17 cells through the induction of SAA1/2 production by intestinal epithelial cells.132 GM-CSF derived from ILC3s sustains the function and survival of myeloid cells, which release IL-1β in response to microbiota.53 IL-1β increases the production of IL-2 by gut ILC3s that are in turn instrumental in the maintenance of induced regulatory T cells.74 b In mucosal draining lymph nodes, MHCII-expressing LTi-like cells suppress the activation or promote the cell death of microbiota-specific T cells through antigen presentation in the absence of co-stimulatory molecules. Highly reactive clones are depleted from the repertoire, thereby promoting peripheral tolerance toward gut microbiota-derived antigens.113 MHCII-expressing ILC3s also control IgA responses against commensal bacteria through interactions with follicular helper T cells (Tfh). Antigen presentation by ILC3s inhibits the production of IL-4 by Tfh and of IgA by B cells. PD1–PDL1 interactions may synergize with antigen presentation to suppress Tfh functions114.
