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| Disease model | IL-17 related finding | Ref. |
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| IL-17A KO mice on C57BL/6 background full-thickness excisional wound healing, males and females | KO mice showed increased myofibroblast numbers and mature collagen with decreased neutrophil infiltration. Delayed healing generated by rIL-17A administration was improved with the addition of neutrophil elastase inhibitor. | [53] |
| Ob/Ob wound healing, males and females | Higher proportion of proinflammatory macrophages to proreparative macrophages in Ob/Ob wounds compared to WT results in delayed wound healing. IL-17A production by proinflammatory macrophages contributed to the delay and was ameliorated with anti-IL-17 antibody. | [72] |
| Ob/Ob wound healing, males and females | Blocking the IL-17A pathway improved wound reepithelialization in Ob/Ob impaired healing model. Further, obese mice with genetic IL-17 family knockout showed reduced proinflammatory macrophages and iNOS but kept proreparative macrophages that express CD206 and LYVE1. | [73] |
| BALB/c full-thickness excisional wound healing, males | Subcutaneous injection of recombinant mouse IL-17 family resulted in increased low-Ly6C macrophage infiltration via proinflammatory mediator levels including MCPs, which produced more type I collagen and delayed wound closure. | [74] |
| BALB/c bone healing, females | Drill injury to the femur in normal and OVX mice showed inhibited healing with anti-IL-17 treatment on day 3 post injury. However, this effect was reversed on days 10 and 21, when groups treated with anti-IL-17 had better healing, especially OVX mice on day 21 post injury. The impact of the IL-17 family on healing was mediated by decreased osteogenic protein expression and increased oxidative stress at the injury site. | [82] |
| BRONJ | BRONJ lesions showed increased IL-17+ cells and IL-17 family in C57BL/6 mice and humans. Lesions also showed increased M1 macrophages, which was attenuated with anti-IL-17A treatment. Exogenous IL-17, subtype not specified, enhanced M1 phenotype and suppressed M2 signaling in murine and human monocytes cultured under polarizing conditions. | [83] |
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