Modulation of skin wound inflammation therapeutically is difficult as macrophages vary in their functions, from pro-inflammatory to pro-healing, making untargeted anti-inflammatory strategies detrimental to wound closure. Our previous gene expression array has shown the dominant role of interleukin 17 (IL-17) in the transition from inflammatory to pro-healing macrophages in wounds. We aimed to identify the function of IL-17 in models of delayed wound healing and asked if its regulation in macrophages was dependent on IL-23. To analyze whether IL-17 was able to modulate inflammation, we compared wounds in multiple mouse models using flow cytometry to observe inflammatory population changes in wound leukocytes and immunofluorescence staining to identify inflammation and inflammatory markers, angiogenesis, wound closure and cell counts. IL-17 deficient obese mice healed significantly faster, and with reduced induced nitric oxide synthase (iNOS) expression than IL-17 expressing obese mice. IL-17 expression was markedly reduced in IL-23but not IL12 deficient mice, shown with both IF staining and RNA analysis. Accelerated wound healing was attributed to increased angiogenesis, however myofibroblast recruitment, differentiation and epidermal closure were not significantly altered. Even through IL-17 expression appears to be dependent on IL-23, IL-23 deficiency was not sufficient to improve wound closure. In conclusion, directly targeting IL-17 in obese mice modelling diabetic wound healing accelerates wound closure by reducing inflammation and improving angiogenesis.