In experimental murine models of autoimmune diseases, including glomerulonephritis [35], myocarditis [36], encephalomyelitis [37], graft-versus-host disease [38], and inflammatory bowel disease [39], inhibiting or knocking out the NLRP3 inflammasome in DCs led to an improvement in disease outcomes, associated with a shift in DCs towards a more tolerogenic/regulatory phenotype [39]. This evidence concerns the gene NLRP3 and inflammatory bowel disease.