Rheumatology Advance Access originally published online on January 11, 2005
Rheumatology 2005 44(7):860-863; doi:10.1093/rheumatology/keh542
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Endothelial cells, fibroblasts and vasculitis
Aims of Therapy/Series Editor: Lorraine Harper
Rheumatology Research Group, Division of Immunity and Infection and 1 Division of Medical Sciences, Institute of Biomedical Research, MRC Centre for Immune Regulation, University of Birmingham, Birmingham B15 2TT, UK.
Correspondence to: C. D. Buckley, Department of Rheumatology, Division of Immunity and Infection, University of Birmingham, Birmingham B15 2TT, UK. E-mail: c.d.buckley{at}bham.ac.uk.
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Abstract |
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One of the most important questions in vasculitis research is not why inflammation of blood vessels occurs but why it persists, often in a site-specific manner. In this review we illustrate how stromal cells, such as fibroblasts and pericytes, might play an important role in regulating the site at which vasculitis occurs. Smooth muscle cells and fibroblasts directly influence the behaviour of overlying vascular cells, amplifying the response of the endothelium to proinflammatory agents such as TNF-
and allowing enhanced and inappropriate leucocyte recruitment. An abnormal local vascular stromal environment can therefore influence local endothelial function and drive the persistence of local vascular inflammation. However, such local vascular inflammation can have distant effects on the systemic vascular system, leading to widespread endothelial cell dysfunction. Vascular endothelial dysfunction is common in a range of immune-mediated inflammatory diseases, is seen in multiple vascular beds, and is reversible following the induction of disease remission. The mechanisms that drive such systemic vascular endothelial dysfunction are unclear but factors such as TNF- and CRP may play a role. Persistence of such widespread endothelial dysfunction in systemic vasculitis appears to have long-term consequences, leading to the acceleration of atherosclerosis and premature ischaemic heart disease. It may also underlie the accelerated atherosclerosis seen in other immune-mediated rheumatic diseases, such as rheumatoid arthritis.
KEY WORDS: Vasculitis
Submitted 1 December 2004;
revised version accepted 10 December 2004.
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