ILC3s promote GALT formation, inflammation, immunity, and homeostasis in the intestine. A progenitor that expresses multiple transcription factors, including PLZF and Id2, responds to IL-7 and differentiates into RORγt-expressing ILC3s (though notably CCR6-expressing/LTi cell progenitors do not express PLZF). Mature ILC3s then integrate multiple environmental cues that modulate their effector functions. These cells are activated by IL-23 produced by myeloid cells through expression of the IL-23R. They can also respond to signals from the microbiota and dietary factors, such as AhR ligands and vitamins. Together, these signals regulate the ability of ILC3s to produce cytokines such as lymphotoxin, IL-17, and IL-22. Three major ILC3 subsets exist, including the CCR6⁺NCR⁻T-bet⁻ LTi and LTi-like cells, the CCR6⁻NCR⁻T-bet⁺ ILC3s, and the CCR6⁻NCR⁺T-bet⁺ ILC3s. ILC3-derived cytokines then promote GALT formation (LTi cells), regulate intestinal homeostasis and inflammation during IBD and in other contexts (CCR6⁻NCR^+/−T-bet⁺ ILC3s), and contribute to protective immunity to intestinal pathogens (CCR6⁻NCR^+/−T-bet⁺ ILC3s). Finally, LTi-like ILC3s express MHC class II, which allows them to interact with and delete commensal-specific CD4⁺ T cells to maintain tolerance of commensal bacterial species and intestinal homeostasis.