Innate Lymphoid Cells: A Link between the Nervous System and Microbiota in Intestinal Networks

Figure 1

The main mechanisms regulating ILCs in IBD. The schematic shows the three ILC subgroup transcription factors and their secretory cytokines, which play proinflammatory (+) or anti- inflammatory (-) roles in IBD, and inhibiting “arrow” means suppression effects on ILCs. Particularly for ILC3s, macrophages secrete IL-1β, which induces RORγt⁺ ILC3s to produce colony stimulating factor 2 (CSF2) (shown by purple arrow). CSF2 then acts on dendritic cells (DCs) and macrophages to promote the secretion of regulatory factors and induce the transformation of immature T cells into mature regulatory T cells (Tregs), which are essential for inhibiting inflammation and maintaining intestinal homeostasis. Natural cytotoxicity receptor^- (NCR^-) ILC3s express high levels of major histocompatibility complex (MHC) II, which is involved in processing and presenting antigens and can limit the response between CD4⁺ T cells and intestinal commensal bacteria, thereby inhibiting inflammation mediated by CD4⁺ T cells to prevent IBD. ILCregs can protect against innate intestinal inflammation by secreting IL-10 to suppress the activation of ILC1s, ILC3s, and autocrine TGF-β1 for the expansion and survival of ILCregs during intestinal inflammation. Furthermore, ILCs could mutually transform via induction by specific cytokines (shown by red font).