狼疮性肾炎
系统性红斑狼疮
免疫学
免疫系统
肾
肾炎
医学
发病机制
巨噬细胞
肾小球肾炎
疾病
病理
生物
内科学
体外
生物化学
标识
DOI:10.1016/j.semnephrol.2006.09.008
摘要
Renal 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.
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