Reducing affinity of αvβ8 interactions with latent TGFβ: dialling down fibrosis

The widely distributed, pleiotropic cytokine TGFβ has a critical role in development, immune function and tissue homeostasis (1), and aberrant TGFβ signalling has been implicated in the pathogenesis of numerous diseases in various organs. Excessive TGFβ signalling has been implicated in a number of fibrotic conditions in the lung including pulmonary fibrosis (2), airway remodelling in asthma (3,4), acute lung injury (5) and chronic obstructive pulmonary disease (COPD) (4). Unfortunately global inhibition of TGFβ leads to severe toxicity (6,7) and therefore there is considerable interest in strategies that can inhibit TGFβ signalling in a cell and tissue specific manner.