Inhibitory effect of anti-malarial agents on the expression of proinflammatory chemokines via Toll-like receptor 3 signaling in human glomerular endothelial cells

Although anti-malarial agents, chloroquine (CQ) and hydroxychloroquine (HCQ) are currently used for the treatment of systemic lupus erythematosus, their efficacy for lupus nephritis (LN) remains unclear. Given that upregulation of glomerular Toll-like receptor 3 (TLR3) signaling plays a pivotal role...

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Veröffentlicht in:	Renal failure 2021-01, Vol.43 (1), p.643-650
Hauptverfasser:	Sato, Riko, Imaizumi, Tadaatsu, Aizawa, Tomomi, Watanabe, Shojiro, Tsugawa, Koji, Kawaguchi, Shogo, Seya, Kazuhiko, Matsumiya, Tomoh, Tanaka, Hiroshi
Format:	Artikel
Sprache:	eng
Schlagworte:	Antimalarials - pharmacology Cell Line Cells, Cultured Chemokine CCL5 - genetics Chemokine CCL5 - metabolism Chemokines Chemokines - genetics Chloroquine Chloroquine - pharmacology Dexamethasone Endothelial cells Endothelial Cells - metabolism glomerular endothelial cells Humans Hydroxychloroquine Inflammation Inflammation - metabolism Interferon-beta - metabolism Kidney Glomerulus - cytology Laboratory Study Lupus Lupus nephritis Lupus Nephritis - drug therapy Malaria Monocyte chemoattractant protein Monocyte chemoattractant protein 1 Monocytes Nephritis Pathogenesis Phosphorylation Poly I-C - metabolism Poly I-C - pharmacology Polyinosinic:polycytidylic acid RNA-directed DNA polymerase Signal Transduction - drug effects Stat1 protein Systemic lupus erythematosus TLR3 protein Toll-like receptor 3 Toll-Like Receptor 3 - genetics Toll-Like Receptor 3 - metabolism Toll-like receptors Western blotting β-Interferon
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