LPS-evoked IL-18 expression in mesangial cells plays a role in accelerating lupus nephritis

Objectives. Systemic lupus erythematosus is occasionally accompanied with bacterial infection. Lipopolysaccharide (LPS) from bacteria can accelerate and exacerbate lupus nephritis (LN) in animal models, but some mechanisms underlying the LPS-induced acceleration are still unclear. First, it is not k...

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Veröffentlicht in:	Rheumatology (Oxford, England) England), 2007-08, Vol.46 (8), p.1277-1284
Hauptverfasser:	Shui, H.-A., Ka, S.-M., Wu, W.-M., Lin, Y.-F., Hou, Y.-C., Su, L.-C., Chen, A.
Format:	Artikel
Sprache:	eng
Schlagworte:	Accelerated LN Animals Apoptosis Autoantibodies - metabolism Biological and medical sciences Cells, Cultured Disease Models, Animal Disease Progression Female Hyperplasia IL-18 Interleukin-18 - biosynthesis Interleukin-18 - genetics Kidneys Lipopolysaccharides - immunology LPS Lupus nephritis Lupus Nephritis - immunology Lupus Nephritis - pathology Medical sciences Mesangial cells Mesangial Cells - immunology Mesangial Cells - pathology Mice Mice, Inbred NZB Nephrology. Urinary tract diseases NF-kappa B - metabolism RNA, Messenger - genetics Translocation, Genetic Up-Regulation - immunology Urinary system involvement in other diseases. Miscellaneous
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