EDITORIAL Transforming growth factor-b: transforming plaque to stability

This editorial refers to ‘Abrogated transforming growth factor beta receptor II (TGFbRII) signalling in dendritic cells promotes immune reactivity of T cells resulting in enhanced atherosclerosis’†, by D. Lievens et al., on page 3717–3727 Lievens and colleagues report an important finding that helps to elu-cidate the role of transforming growth factor b (TGFb)b in athero-sclerotic plaque formation.1 TGFb is a widely expressed cytokine produced by smooth muscle cells, endothelial cells, monocytes, macrophages, and T cells.2,3 Clinical studies suggest that TGFb is antiatherosclerotic, citing a negative correlation between plasma TGFb concentration and the extent of atherosclerosis.4–7 In mouse models of atherosclerosis, inhibition of TGFb signalling causes the formation of unstable plaques. This plaque phenotype is probably caused by two consequences of inhibiting TGFb: first