Vasculopathy and vasculitis in systemic lupus erythematosus

Abstract

Systemic lupus erythematosus (SLE) is an autoimmune connective tissue disease, where vascular lesions are one of the typical symptoms. The pathological process often involves skin vessels, renal glomeruli, the cardiovascular system, brain, lung alveoli, and gastrointestinal tract vessels. This review presents possible adverse mechanisms underlying the cause and effect relationship of various factors causing vascular lesions in SLE patients. The generally accepted hypothesis links vascular damage in SLE with the deposition of immune complexes in the vascular endothelium. The anti-endothelial cell antibodies (AECA), antiphospholipid antibodies and anti-double stranded DNA antibodies present in SLE, that directly or indirectly affect endothelial cells, causing inflammatory damage to the vessel wall, and their role, have been discussed. It has been stressed that although the suggested role of AECA in vasculitis pathogenesis has not been fully established, evidence, however, has demonstrated that AECA is a factor causing endothelial damage in SLE patients. On the other hand, issues concerning cellular adhesion molecules which enable leukocyte adhesion and rolling along the endothelial cell surface, and their extravascular migration, focus on the role they may be playing in SLE patients with vasculitis. A potential role of soluble forms of adhesion molecules, pentraxin 3, medications, infections in the pathogenesis of this disease has also been shown. Special attention has been given to the role of type 3 hepatitis virus in vascular damage in SLE.

Immune complexes activate human endothelium involving the cell-signaling HMGB1-RAGE axis in the pathogenesis of lupus vasculitis

“…6,7 Recent studies on lupus vasculitis and nephritis showed that activated monocytes and macrophages vigorously participate in, and amplify inflammation, which influences the outcome of the condition. [33][34][35] In these experiments, transwell chambers were used to detect the effect of IC-pretreated CRL-1730 cells and the transendothelial migration of U937 cells as compared with negative control CRL-1730 cells.…”

“…6,7 Vasculopathy and vasculitis could be associated with the deposition of ICs on endothelium, leading to endothelial cell activation and inflammatory cell infiltration into the inflammatory sites. [6][7][8][9] However, the effects of ICs on endothelial cells and the potential mechanisms involved remain unclear.…”

Wpływ wybranych cytokin na uszkodzenie narządów w toczniu rumieniowatym układowym

“…Również częściej występują zmiany skórne w postaci siności siatkowatej (livedo reticularis), ponadto niedokrwistość, przyspieszone OB oraz często stwierdza się obecność przeciwciał anty-SS-B [19]. Epizod zapalenia naczyń może się rozwinąć na skutek odkładania się kompleksów immunologicznych w ścianie naczynia, ale również wskazuje się na rolę przeciwciał przeciwko komórkom śródbłonka (antiendothelial cell antibodies -AECA), które prowadzą do ich bezpośredniego uszkodzenia [21]. Obecność przeciwciał AECA stwierdza się nawet u 80% chorych na TRU [22].…”

Accelerated Atherosclerosis in Patients with Systemic Lupus Erythematosus and the Role of Selected Adipocytokines in This Process

“…[14]. Vascular disease in SLE patients can occur due to a combination of diferent pathological processes, for example, atherosclerosis, cloting disorders, and systemic vasculitis associated with vascular wall injury (especially endothelial dysfunction), caused by an autoimmune process [24,28].…”

“…SLE patients most typically exhibit cutaneous vasculitis; systemic vasculitis develops in 10-18% of these patients and, as a life-threatening condition, may require aggressive therapy [14,15].…”