While the current study did not directly examine IL17, evidence for a dysfunctional T-cell-microbe crosstalk in CNS disorders was provided in the context of experimental autoimmune encephalomyelitis (EAE, a model of multiple sclerosis, [46]) and maternal immune activation (MIA, a model of autism, [47,48,49]), where induction of the T helper 17 (Th17)/IL-17a pathway by members of the gut microbiota elicited cortical and behavioral abnormalities. The gene discussed is IL17A; the disease is central nervous system disorder.