The resistance of VPAC1 KO mice to inflammatory insult in the DSS colitis and EAE models is reminiscent of that found in mice deficient in VIP (the ligand) in EAE and other models of inflammation such as TNBS-induced colitis and endotoxemia induced by a lethal dose of LPS, a model of acute inflammation with no Th1/Th17 implication [34–36]. Here, VIPR1 is linked to serum lipopolysaccharide activity.