Schematic representation of the source and roles of TGF-β₁ and TGF-β₂ in OVA-induced airway inflammation and remodelling.

<p>Following OVA sensitisation and challenge there appears to be a shift in the localisation/production of TGF-β₁ (A) and TGF-β₂ (B) away from bronchial epithelial cells with increased localisation/production of TGF-β₁ to macrophages and TGF-β₂ to macrophages and eosinophils. TGF-β₁ and TGF-β₂ are potent inhibitors of bronchial epithelial proliferation, the reduced localisation of TGF-βs to these cells may be directed towards epithelial proliferation and repair. However, greater levels of inflammatory cell derived TGF-β may counteract this. TGF-β₁ is capable of inducing epithelial-mesenchymal transition of bronchial epithelial cells <i>in vitro</i> but whether this occurs in this model or asthmatic airways is uncertain. TGF-β₁ plays a critical role in the recruitment/maintenance of macrophages and the synthesis/deposition of decorin as well as contributing to the recruitment/maintenance of eosinophils, lymphocytes and synthesis/deposition of collagen. TGF-β₂ appears to have a more restricted role, contributing to the recruitment/maintenance of eosinophils, lymphocytes and the synthesis/deposition of collagen. Red arrows denote synthesis/localisation of TGF-β isoforms, blue illustrates functions of the isoforms based on this study and the literature. The width of the arrows symbolise the apparent relative importance of the source of that isoform or its function.