کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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3897589 | 1250262 | 2007 | 10 صفحه PDF | دانلود رایگان |
SummaryRenal disease is the major cause of morbidity in patients with lupus. MRL-Faslpr mice share features with human lupus. The tempo, predictability, and homogeneous expression of disease in MRL-Faslpr mice make them an excellent tool to probe the pathogenesis of lupus nephritis and to identify therapeutic targets. This article focuses on the concepts that renal parenchymal cells are active participants that regulate immune responses in the kidney, and that the interaction between parenchymal cells and leukocytes (macrophages, T cells) determine whether the kidney is protected or destroyed during lupus nephritis. In particular we review the role of macrophages, fueled by the principal macrophage developmental molecule, colony stimulating factor-1, in lupus nephritis, and we review T cells and costimulatory pathways and the interaction of these leukocytes with renal parenchymal cells that regulate lupus nephritis.
Journal: Seminars in Nephrology - Volume 27, Issue 1, January 2007, Pages 59–68