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Transforming growth factor-β: transforming plaque to stability

Kevin Tse, Klaus Ley
DOI: http://dx.doi.org/10.1093/eurheartj/ehs228 3684-3686 First published online: 27 July 2012

This editorial refers to ‘Abrogated transforming growth factor beta receptor II (TGFβRII) 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 elucidate the role of transforming growth factor β (TGFβ)β in atherosclerotic plaque formation.1 TGFβ is a widely expressed cytokine produced by smooth muscle cells, endothelial cells, monocytes, macrophages, and T cells.2,3 Clinical studies suggest that TGFβ is antiatherosclerotic, citing a negative correlation between plasma TGFβ concentration and the extent of atherosclerosis.47 In mouse models of atherosclerosis, inhibition of TGFβ signalling causes the formation of unstable plaques. This plaque phenotype is probably caused by two consequences of inhibiting TGFβ: first, blockade of TGFβ's role in promoting plaque fibrosis would make the plaques less stable, and, secondly, the absence of TGFβ signalling results in increased numbers of pro-inflammatory T cells that populate atherosclerotic lesions.812 Because dendritic cells (DCs) express the TGFβ receptor (TGFβR) and have a central role in regulating immune responses, studying the potential role of the TGFβR in DCs and how it might influence T-cell activation and modulate atherosclerosis is an area of great interest.

To study the effect of TGFβ signal inhibition on DCs and its eventual effect on atherosclerosis development, Lievens et al. backcrossed Apoe–/– mice with mice whose TGFβ-β signalling in DCs is disrupted by a dominant negative TGFβRII transgene (that encodes the extracellular and transmembrane, but not intracellular, regions of the TGFβ type II receptor) inserted into the CD11c promoter.1 CD11c is expressed on most mouse DCs and some macrophages, and …

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