Deletion of IL-17D in non-hematopoietic compartments was sufficient to replicate the phenotype observed in IL-17D-deficient animals, while the effects of IL-17D deletion in the hematopoietic compartment were minimal, suggesting that IL-17D secretion from non-hematopoietic compartments is required for the pathogenic effects of IL-17D during bacterial infection. Here, IL17D is linked to bacterial infectious disease.