IL17A and metabolic dysfunction-associated steatohepatitis: Temporal studies indicated that Th17 cells initiate NASH development and contribute to progression, while Th22 cells demonstrated dual roles in cytoprotective and toxic functions: in the absence of IL-17, Th22 cells infiltrated liver to attenuate the hepatic lipotoxicity, but in the presence of hepatic IL-17, Th22 cells are not able to counteract IL-17-mediated liver damage (87).