Recent work on the role of γδ T cells and IL-17 in pulmonary fibrosis suggests that γδ T cells amplify a Th17 response and promote inflammation, but differ on whether they amplify collagen deposition [32], help to control fibrosis via production of CXCL10 or IL-22 [32], [49]–[51] or have no effect on fibrotic disease [33]. This evidence concerns the gene IL17A and pulmonary fibrosis.