1,721,331 research outputs found
Renal interstitial cells, proteinuria and progression of lupus nephritis: new frontiers for old factors.
No full textInterstitial cells, inflammatory-immune cells, tubular cells and endothelial cells of the peritubular capillaries have arisen as possible major players of the nephron damage in lupus nephritis. Increased ICAM-1, Von Willebrand factor, soluble endothelial protein C receptors and decreased ADAMS-13 point to a diffuse vascular damage. Albuminuria elicits a rapid generation of hydrogen peroxide in proximal tubular cells along with nuclear factor-kB activation, endothelin-1 and transforming growth factor (TGF-beta1) upregulation. TGF-beta1 enhances epithelial-to-mesenchymal transdifferentiation. Albuminuria also enhances the expression of macrophage chemotactic protein-1 and macrophage inflammatory protein-1alpha, thus leading to increased interstitial inflammation. TGF-beta1 and thrombospondin-1, a putative activator of TGF-beta, induce apoptosis of peritubular capillaries, as well as of glomerular endothelial cells. All these events can be counteracted by hepatocyte growth factor (HGF), which is expressed by the epithelial tubular cells and stimulates the growth of epithelial cells (mitogen), enhances the motility of epithelial cells (motogen), induces renal epithelial tubule regeneration (morphogen) and enhances angiogenesis (angiogen). The balance between TGF-beta1 and HGF could be a key to define the prognostic value of kidney histopathology at baseline and during follow-up, in lupus nephritis. Therapeutic strategies aiming at altering the biological balance in the patients are at hand to test and prove the experimental evidences
Association between DR antigens, rheumatoid arthritis with and without features and systemic lupus erythematousus in northern Italy.
No full textJ RHEUMATO
B-cell lymphomagenesis and human autoimmune models.
No full textAbstract
The concept that B-cell lymphomagenesis represents a multistep process is widely accepted. Pathogenetic events should be better defined both in early and late stages of lymphoproliferation. In the past few years, novel study approaches have been focused on understanding the mechanisms of lymphomagenesis. In particular, immune stimulation by infectious agents or autoantigens, T-cell help, altered immunocompetence, and local cytokine networks seem to be crucial in favouring B-cell expansions. In turn, actively proliferating B cells are at higher risk of undergoing genetic alterations that make the clone capable of fully autonomous growth, i.e., fully neoplastic. Peculiar human autoimmune diseases predisposing to B-cell lymphoma represent relevant models to characterize and dissect the temporal sequence of the different lyphomagenetic events. The present review, particularly, focuses on Sjoegren's syndrome, and on recent findings regarding the putative role of hepatitis C virus in B-cell lymphoproliferation. The biologic and clinical implications may be of major relevance for other B-cell disorders characterized by higher prevalence and morbidity
B lymphocyte stimulator (BLyS) and monocytes: possible role in autoimmune diseases with a particular reference to rheumatoid arthritis
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Similarity of the genetic background in rheumatic diseases between northen patients.
No full textANN RHEUM DI
RAASI, NSAIDs, antidiabetics, and anticoagulants: More data needed to be labeled as harmful or neutral in SARS-CoV-2 infection
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ACR70-disease activity score remission achievement from switches between all the available biological agents in rheumatoid arthritis: a systematic review of the literature.
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