XXXX are associated with aberrant expression of @entity806 and decay accelerating factor in vascular endothelium.

@entity1 @entity32 @entity1009 @entity75 @entity1252 @entity2631 @entity1504 @entity806 @entity9819 @entity785
One of the main features of systemic and localized forms of @entity2631 is @entity1504 , the mechanism of which is not yet understood. Recently, we have shown undetectable or decreased expression of complement regulatory molecules, @entity806 ( @entity806 ) and @entity9819 ( @entity9819 ), in cutaneous endothelium of @entity1 with @entity785 ( @entity785 ). In some @entity1 , @entity1009 expression in endothelium was also altered. As these molecules protect endothelial cells from damage by autologous complement, their decreased expression could be part of the mechanism of @entity1504 in @entity785 . In the present study, we investigated the expression of @entity806 , @entity9819 and @entity1009 in the endothelium of lesional and non-lesional skin of @entity1 with localized morphoea. Normal skin and lesional skin from @entity1 with @entity1252 , and three @entity32 , were included as relevant controls. The results showed that the extent of expression of the three molecules in non-lesional skin of @entity1 with morphoea, on all the skin cells and structures, was identical to that of normal skin. In lesional skin, however, the expression of @entity806 and @entity9819 in endothelium was either undetectable or only present to a very slight degree. @entity1009 expression in endothelium in lesional skin was normal. No such aberrant expression was observed in the lesions of any of the control diseases. These results indicate a decreased ability of endothelial cells in lesional areas to protect themselves from autologous complement, and this could contribute to @entity1504 in @entity75 .
