Circulating endothelial cells and vascular injury in systemic lupus erythematosus
Author:
Publisher
Springer Science and Business Media LLC
Subject
Rheumatology
Link
http://link.springer.com/content/pdf/10.1007/s11926-996-0067-6.pdf
Reference25 articles.
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3. Lozada C, Levin RI, Huie M, et al.: Identification of C1q as the heat-labile serum cofactor required for immune complexes to stimulate endothelial expression of the adhesion molecules E-selectin and intercellular and vascular cell adhesion molecules 1. Proc Natl Acad Sci U S A 1995, 92:8378–8382. A seminal finding, which in part explains the development of immune-complex-mediated vasculitis. Immune complexes fix C1q, and the complex interacts with the C1q receptor to stimulate endothelial expression of adhesion molecules.
4. Belmont HM, Buyon J, Giorno R, et al.: Up-regulation of endothelial cell adhesion molecules characterizes disease activity in systemic lupus erythematosus. The Shwartzman phenomenon revisited. Arthritis Rheum 1994, 37:376–383. This paper describes a relationship between the occurrence of endothelial cell activation in otherwise "healthy" patient tissue and disease activity, providing vidence that vascular tissue is primed for tissue injury.
5. Cronstein BN, Kimmel SC, Levin RI, et al.: A mechanism for the antiinflammatory effects of corticosteroids: the glucocorticoid receptor regulates leukocyte adhesion to endothelial cells and expression of endothelial-leukocyte adhesion molecule 1 and intercellular adhesion molecule 1. Proc Natl Acad Sci U S A 1992, 89:9991–9995. This article provides an explanation for the efficacy of corticosteroids in the treatment of acute flares of SLE. Corticosteroids prevent the activation-dependent expression of adhesion molecules in cultured endothelial cells.
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