In conclusion, the studies here reported clearly demonstrate that susceptibility to PCM is mainly mediated by the proinflammatory IFN-γ-IDO axis of innate responses, whereas resistance relies on the initial anti-inflammatory TGF-β-pIDO-Treg axis that confers a sustained tolerogenic phenotype in pulmonary DCs allowing A/J mice to interact with a primary fungal pathogen as a commensal microbe. Here, TGFB1 is linked to paracoccidioidomycosis.