A New Role for CD11c+ Myeloid Cells in Hypertension
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See related article, pp 709–718
In recent years, cumulating evidence has suggested that inflammation plays a key role in the development and maintenance of arterial hypertension. Hypertension is associated with infiltration and accumulation of both innate and adaptive immune cells into the vasculature, kidney, and heart where they release cytokines and promote oxidative stress and tissue (mal)adaptation. Myeloid cells like monocytes, macrophages, and dendritic cells are components of the innate immune system that are particularly relevant to cardiovascular diseases. Blood pressure and vascular remodeling in response to angiotensin II (AngII) or deoxycorticosterone acetate salt has been shown to be reduced in mice with functionally-deficient macrophages.1 Rickard et al2 have demonstrated that mineralocorticoid receptors regulate monocyte/macrophage function, and mineralocorticoid receptor deletion from LysM+ myelomonocytic cells protects against deoxycorticosterone acetate salt-induced cardiac fibrosis and increased blood pressure.
In the current issue of Hypertension, Hevia et al3 add to our understanding of the major importance of innate immune cells in hypertension. They provide new evidence that CD11c+ myeloid cells might play an essential role in high blood pressure.3 CD11c is an integrin α X chain protein. CD11c+ cells are widely regarded to be dendritic cells, but also monocytes, macrophages, neutrophil granulocytes, and even B cells and some T cells can express CD11c. Both activated macrophages and dendritic cells can present antigen and likely produce similar …