ILC3s can express MHC-II to present microbiota-related antigens to commensal-specific CD4+T cells, leading to cell death and immune tolerance, and this process is dysregulated in patients with inflammatory bowel disease [17], but CCR6+ILC3 cells also accumulate in the inflamed joints of patients with RA and mice with CIA, where they produce IL-17 and IL-22 [18]. This evidence concerns the gene IL17A and rheumatoid arthritis.