TGFB1 and pulmonary fibrosis: Importantly, IL-23p19 and IL-17A are upstream of the expression of TGF-β1 the central mediator of lung fibrosis suggesting that innate IL-17A from γδ T cells [26] might promote the commitment towards an inflammatory Th17 phenotype through induction of TGF-β1 in an IL-6 rich environment.