Abstract Blockade or genetic deletion of IL-17RA resulted in marked increases in IL-17 response by T-cells. We hypothesize that the hyper Th17 response in IL-17 deficient mice is due to alterations of the gut microbiome particularly overgrowth of segmented filamentous bacteria (SFB). Our data shows that Il17ra-/- and Il17rc-/- mice have overgrowth of SFB (10 fold higher than WT.Taconic), suggesting a critical role of IL-17 signaling in SFB colonization. Higher SFB colonization in Il17ra-/- and Il17rc-/- mice results in expansion of IL-17A and IL-22 producing Th17 cells. As further evidence that this expansion was not T-cell intrinsic, we observed similar frequencies of IL-17 producing cells in WT and Il17ra-/- when naïve T-cells were polarized in vitro to Th17 cells. Furthermore, vancomycin depletion of SFB in Il17ra-/- mice resulted into fewer Th17 cells in the lamina propria and spleen, suggesting gut microflora responsible for hyper Th17 response. SFB-colony free WT mice with intact IL-17 signaling can control SFB overgrowth but IL-17 deficient mice could not following SFB inoculation. To further define the role of IL-17 in SFB colonization, we have generated SFB-free Il17ra conditional knockout (Il17rafl/flxe2a cre) mice. SFB-free Il17rafl/flxe2a cre mice are devoid of hyper Th17 responses, and SFB inoculation resulted into acquisition of hyper Th17 phenotype as observed in Il17ra-/-. Our data suggest that IL-17 signaling regulates SFB colonization and associated Th17 responses.