[The role of endothelial cells in the pathogenesis of systemic lupus erythematosus].

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease affecting connective tissue. It is characterized by a variety of clinical symptoms. In the pathogenesis of SLE, genetic as well as environmental and hormonal factors are considered to be responsible for the development of multiple immunological phenomena. Recently, the process of angiogenesis and vasculogenesis and their dysfunction has been considered in the pathogenesis of SLE. Vascular lesions seem to be responsible for the cutaneous, nephritic, cardiovascular, and gastrointestinal symptoms. Besides the typical antinuclear antibodies, anticardiolipin, anti-CRP, and antiendothelial cell antibodies are also present in the serum of SLE patients. Recently, antiendothelial cell antibodies (AECAs) have greatly aroused the interest of researchers. An increased titer of AECAs is assumed to be a vascular damage marker. It seems that AECAs can be responsible for vascular damage in SLE, thus confirming the strong relationship between SLE activity and AECA titers. In SLE patients' blood samples, increased levels of circulating endothelial cells (ECs) were also found. At the same time, higher adhesive molecule expression was detected at the inflammation site as well as in the healthy skin, which may indicate general endothelial cell activation. Positive correlation between EC count, C3 complement, and anticardiolipin antibodies and disease activity was also demonstrated. The above observations show the great impact of the vascular endothelium in the pathogenesis of SLE. There is an urgent need to continue further research on this subject.