Correlations between concentrations of interleukin (IL)-17A, IL-17B and IL-17F, and endothelial cells and proangiogenic cytokines in systemic lupus erythematosus patients.

Systemic lupus erythematosus (SLE) is an autoimmune disease of multifactorial pathoaetiology. Different organs and blood vessels may be affected by chronic inflammation. A direct cause of the disease has not yet been found, so research is being carried out to this effect. The role of the recently identified helper T lymphocyte CD4+, described as Th17, and its dependent cytokines have been of particular interest. The aim of the study was to evaluate IL-17A, IL-17B, IL-17F and IL-23 in 60 SLE patients and 26 age-matched, healthy volunteers and also to investigate the correlation between levels of the investigated cytokines and VEGF, PIGF, as well as number of endothelial cells. IL-17A, IL-17B, IL-17BR and IL-17F levels were found to be higher in SLE patients than in the control group. However, only IL-17F levels showed a statistically significant correlation with the number of endothelial cells (aCEC) and disease activity. Correlations between levels of IL-17F and VEGF and PIGF as well as VEGF and IL-17A and IL-23 were statistically significant. Increased levels of the selected cytokines from the IL-17 family in SLE patients suggest a role for them not only in the inflammatory process but also in angiogenesis. This also highlights the role of IL-17F in activating vascular endothelial cells and consequently blood vessel formation, and in the relationship between the inflammatory reaction and angiogenesis in the development of SLE.

[The role of endothelial cells in the pathogenesis of systemic lupus erythematosus]. / Rola komórek sródblonka w patogenezie ukladowego tocznia rumieniowatego.

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.

[Drug-induced lupus erythematosus and systemic lupus erythematosus--differences and similarities]. / Toczen indukowany lekami a ukladowy toczen rumieniowaty--róznice i podobienstwa.

Drug-induced lupus (DIL) is a lupus-like syndrome. Its clinical and laboratory features are very similar to idiopathic lupus. First description of DIL is from 1945. Since that time over 80 medications are known to be responsible for development of the disease. Nevertheless mechanisms responsible for this process are not known enough. Nowadays direct and indirect mechanisms in DIL are known. The slow acetylator status has an important position. Moreover the role of estrogens and anti-TNF-alpha therapy are taken into consideration. The T cells' participation and the methylation of DNA and their role in graft-vs.-host disease, which is the murine model for DIL, are considered among others. Researches point also to the LFA-1 and the IL-6 as factors responsible for DIL's development. Another element which could be significant in this process is the presence of antimielo-peroxydase antibodies. Also the role of disruption of T-cell maturation in the thymus induced by the drugs' metabolites may have an important position. Nevertheless it is still very hard to say which of those mechanisms is the main one. In spite of everything it's not clear enough if the observed clinical manifestations are caused by drugs/their metabolites,- DIL or that they are consequences of a induction of silent process leading to SLE development.