2002
DOI: 10.1016/s1568-9972(02)00063-0
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Antiendothelial cell antibodies in systemic lupus erythematosus

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Cited by 76 publications
(58 citation statements)
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“…The generation of autoAbs cross-reactive with endothelial cells is involved in several autoimmune vascular diseases [33][34][35] . Our studies [23,[36][37][38] showed that Abs directed against DV NS1 cross-reacted with endothelial cells and induced these cells to undergo nitric oxide-mediated apoptosis as well as cytokine and chemokine production.…”
Section: Discussionmentioning
confidence: 99%
“…The generation of autoAbs cross-reactive with endothelial cells is involved in several autoimmune vascular diseases [33][34][35] . Our studies [23,[36][37][38] showed that Abs directed against DV NS1 cross-reacted with endothelial cells and induced these cells to undergo nitric oxide-mediated apoptosis as well as cytokine and chemokine production.…”
Section: Discussionmentioning
confidence: 99%
“…It is possible that endothelial apoptosis, secondary to autoimmune injury, could initiate dysfunctional endothelial cell proliferation that culminates in PAH in the same manner that endothelial apoptosis, induced by vascular endothelial growth factor antagonism, results in endothelial cell proliferation and PAH [67]. Anti-endothelial antibodies are present in autoimmune disorders associated with PAH including systemic lupus erythematosus [68], mixed connective tissue disease [69] and scleroderma [38]. In lupus and Sjö gren's syndrome, antibody and complement deposits are localised in the walls of pulmonary arteries of patients with PAH [70,71].…”
Section: Autoreactive B-cell Activation In the Absence Of T-cell Regumentioning
confidence: 99%
“…Notably, inflammation in the perivascular space includes accumulation of mast cells and lymphocytes (11,14,15). Given the association of autoimmune phenomena with SPH, such as detection of anti-nuclear and anti-endothelial cell antibodies (16)(17)(18)(19)(20)(21), the finding of antibody-complement deposits in the lungs of patients with SPH (22,23), and the presence of inflammatory cells around plexiform lesions in SPH, there appears to be a basis for an immune-mediated component in SPH pathogenesis. We sought to specifically address the contribution of T cells to the development of SPH.…”
mentioning
confidence: 99%