IL17A and infection: Subsequently, the team further observed that MIA-induced ASD offspring rats were more susceptible to intestinal inflammation after the infection with Citrobacter rodentium, and in contrast to the prenatal role of the MIA in neurodevelopmental phenotype, IL-17 mediated an altered naïve CD4+ T chromatin landscape postnatally by modifying the maternal gut microbiota to modulate the offspring’s immune-related phenotype (76).