Adhesion molecules, sex steroids, and the pathogenesis of vasculitis syndromes.
The pathogenesis of the vasculitis syndromes slowly continues to yield its secrets. Over the past year, evidence has continued to accumulate, indicating that the endothelium exhibits a wide range of regulatory functions, mediated in large part through adhesion molecules. Several studies showed increased expression of such molecules in vasculitis. New appreciation of the Shwartzman reaction, which could explain non-immune complex-mediated vascular inflammation, continues to mount and to point toward potential future therapies. Soluble adhesion molecules were studied as potential diagnostic tools and/or markers of disease activity. Anti-endothelial cell antibodies (AECA) remain controversial as potential mediators of vasculitis. The results of recent studies suggest that AECA may be seen more frequently in ANCA-negative vasculitis and that AECA possess unique antigenic specificities in Wegener's granulomatosis and systemic lupus erythematosus. Sex steroids were shown to affect the expression of endothelial adhesion molecules, in addition to possessing well documented immunoregulatory properties. These findings may point to a critical role for sex steroids in the pathogenesis of vasculitis syndromes with female predominance, particularly Takayasu's arteritis.
van Vollenhoven
R F
RF
Division of Immunology and Rheumatology, Stanford University Medical Center, CA 94305, USA.
D000818:Animals; D000906:Antibodies / Q000276:immunology; D015815:Cell Adhesion Molecules / Q000502:physiology*; D004730:Endothelium, Vascular / Q000276:immunology / Q000502:physiology; D005260:Female; D012739:Gonadal Steroid Hormones / Q000502:physiology*; D006801:Humans; D013577:Syndrome; D014657:Vasculitis / Q000209:etiology*
D000906:Antibodies; D015815:Cell Adhesion Molecules; D012739:Gonadal Steroid Hormones