Host defenses against Histoplasma capsulatum require the action of several cytokines. Here, we explored the influence of interleukin (IL)–17 and IL‐23 on immunity to H. capsulatum infection in mice. In lungs, synthesis of IL‐17 was up‐regulated during acute infection, and the cells producing it were predominantly CD3⁺. Neutralization of IL‐17A blunted fungal clearance but did not promote progressive infection. Decreased inflammatory cell recruitment and increased levels of IL‐6 and IL‐10 were associated with impaired clearance. To determine whether the elevated cytokine levels were important in the action of IL‐17A, IL‐6^−/− or IL‐10^−/− mice were treated with anti–IL‐17A; neutralization of IL‐17A did not alter fungal burden in either group of knockout mice. We explored the relationship between IL‐17 and IL‐23 because they have been reported to form a regulatory network. IL‐23 transcription and protein level were increased in the lungs of infected mice. Mice producing IL‐23 in the absence of IL‐12 manifested prolonged survival that was IL‐17 dependent. Thus, IL‐17 is requisite for the generation of optimal inflammatory and protective responses. Generation of functional IL‐17⁺ cells is dependent on IL‐6 and IL‐10. Our findings also establish the existence a regulatory IL‐17/IL‐23 axis in histoplasmosis.