This article appears in the following Rheumatology issue: Update in systemic sclerosis [View the issue table of contents]
The microvascular endothelium in scleroderma
1Division of Rheumatology and Immunology, University of Toledo College of Medicine, Toledo, OH, USA.
Correspondence to: B. Kahaleh, Division of Rheumatology and Immunology, University of Toledo College of Medicine, 3120 Glendale Ave., Toledo, OH 43617, USA. E-mail: bashar.kahaleh{at}utoledo.edu
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Abstract |
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Vascular endothelial injury in SSc leads to a host of pathological changes in the blood vessels that adversely impact the physiology of many organ systems and eventually results in a state of chronic tissue ischaemia. Current hypotheses in SSc vascular disease pathogenesis suggest a possible infectious or chemical trigger(s) that activates both cellular and humoral immunity. Products of immune activation may lead to vascular injury possibly through the production of autoantibodies and the release of products of activated T cells that can directly damage the endothelium. Knowledge of the initial trigger of immune activation in SSc may offer an opportunity to develop a multiple step strategy for therapeutic intervention.
KEY WORDS: Scleroderma, Scleroderma vascular disease, Endothelial cells, Raynaud's phenomenon, Endothelial apoptosis, Cytomegalovirus, Anti-endothelial antibodies
Submitted 30 April 2008; Accepted 19 June 2008