TGFB1 and pemphigus foliaceus: During the pathological progression of PF, an excessive polarization of macrophages towards the M1 phenotype leads to epithelial cell demise, while uncontrolled infiltration of M2 macrophages in the lungs results in the release of a multitude of profibrotic cytokines, including IL-1β, tumor necrosis factor-alpha (TNF-α), TGF-β, platelet-derived growth factor (PDGF), and fibroblast growth factor receptor (FGFR) [40–42].