FIGURE 2.

Novel potential therapeutic targets in interstitial lung disease. Matrix metalloproteinase 9 (MMP9) blockade with the monoclonal antibody, andecaliximab, led to response in lungs with a type I interferon‐rich environment with increased concentrations of CXCL10 (CXC motif chemokine ligand 10) and by reducing transforming growth factor beta (TGFβ) signalling and decreasing fibrotic extracellular matrix (ECM) deposition. Epithelial–mesenchymal transition (EMT) creates an environment facilitating fibrosis following alveolar epithelial cell injury. ²² IL‐23‐induced EMT is dependent on mammalian target of rapamycin (mTOR) signalling and can be reversed by rapamycin, ²³ or potentially targeted blockade by anti‐IL‐23 antibody which can attenuate airway inflammation in acute exacerbations. ²⁴ Stearic acid reduced the TGFβ‐induced expression of α‐smooth muscle actin (αSMA) and collagen type 1 (Col1a1) in fibroblasts, indicating potential novel antifibrotic properties. ²⁶ Recent studies of IL‐13 blockade using the monoclonal antibody, lebrikizumab, was demonstrated to be well tolerated and safe, but lebrikizumab alone or in combination with pirfenidone did not reduce the rate of forced vital capacity ⁸⁷