To summarize, direct and indirect transwell co-cultures and conditioned medium studies show that B cell-fibroblast crosstalk in IPF results in the upregulation of fibrotic proteins (e.g., α -SMA, fibronectin and PAI1), whereas T cell-fibroblast interactions in IPF are diverse, with increased fibrotic markers on one hand and a potential protective mechanism that cause decreased fibrotic changes on the other hand. This evidence concerns the gene SMN1 and idiopathic pulmonary fibrosis.