Abstract

This editorial refers to ‘Mast cells in human carotid atherosclerotic plaques are associated with intraplaque microvessel density and the occurrence of future cardiovascular events’, by S. Willems et al. , doi:10.1093/eurheartj/eht186 Atherosclerosis in the presence of hyperlipidaemia is considered today as an inflammatory disease of the arterial wall. The dominant inflammatory cell is the macrophage; however, interaction with other inflammatory cells and red cells may be critical in the outcome of the plaque, i.e. whether plaques remain stable or become unstable. It has been repeatedly shown that macrophage interaction with T cells and dendritic cells is critical for the progression of plaques and for maintaining and sustaining inflammation. The role of mast cells in atherosclerosis has only been studied sporadically, and that too mostly in the aortic and coronary beds. Willems et al .1 now show for the first time not only that severe carotid atherosclerotic disease is associated with a high number of mast cells but that the instability of the plaque may be influenced by the number of mast cells and their state of activation, which probably contribute to angiogenesis and plaque haemorrhage. Also, patients with high intraplaque mast cells had significantly greater cardiovascular events during a 3-year follow-up. However, the basic mechanisms involved will need further study in both animal models and man. Paul Ehrlich's doctoral thesis was a milestone in the study of mast cells, and he noted that they had similar staining characteristics to basophils, demonstrating metachromatic staining with aniline dyes.2 Mast cell development depends on the expression of KIT ligand, also known as mast/stem cell growth factor (SCF), receptor from the pluripotent haematopoietic progenitor cells (HPCs) that express CD34 + , CD117 + , CD13 + , FcɛRI – , maturing in the target tissues, such as skin, mucosal surfaces, and probably also …

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