Leukocyte-renal epithelial cell interactions regulate lupus nephritis.
Renal disease is the major cause of morbidity in patients with lupus. MRL-Fas(lpr) mice share features with human lupus. The tempo, predictability, and homogeneous expression of disease in MRL-Fas(lpr) 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.
Kelley
Vicki Rubin
VR
Renal Division, Department of Medicine, Brigham and Women's Hospital/Harvard Medical School, Boston, MA 02115, USA. vkelly@rics.bwh.harvard.edu
D000818:Animals; D015703:Antigens, CD / Q000502:physiology; D017209:Apoptosis; D060890:B7-H1 Antigen; D002450:Cell Communication; D004847:Epithelial Cells / Q000502:physiology; D006801:Humans; D007668:Kidney / Q000166:cytology*; D007684:Kidney Tubules / Q000473:pathology; D008181:Lupus Nephritis / Q000209:etiology*; D016173:Macrophage Colony-Stimulating Factor / Q000502:physiology; D008264:Macrophages / Q000502:physiology*; D013601:T-Lymphocytes / Q000502:physiology*
D015703:Antigens, CD; D060890:B7-H1 Antigen; C423236:CD274 protein, human; D016173:Macrophage Colony-Stimulating Factor