狼疮性肾炎
趋化因子
免疫学
人口
肾炎
发病机制
细胞因子
肾小球肾炎
单核细胞
系统性红斑狼疮
免疫系统
生物
医学
肾
疾病
病理
内分泌学
环境卫生
作者
Marco Tucci,Nicola Calvani,Hanno B. Richards,Cosima Quatraro,Franco Silvestris
标识
DOI:10.1196/annals.1361.084
摘要
Abstract: Lupus nephritis (LN) occurs in more that one-third of patients with systemic lupus erythematosus. Production of nephritogenic autoantibodies, glomerular immune complex deposition, and cytokine overproduction have been postulated to contribute to the pathogenesis of LN. However, overexpression of chemokines and imbalance of dendritic cell (DC) homeostasis may contribute to the development of nephritis in SLE. We present evidence that monocyte chemoattractant protein (MCP)-1 promotes renal disease in experimental glomerulonephritis, while its increased urinary levels reflect the severity of the disease in humans. Although macrophages are the prevalent infiltrating population within the kidney, it has been recently proposed that several chemokines and related receptors expressed by DCs may divide this cell population into myeloid (mDC) and plasmacytoid (pDC) subsets. However, the chemokine receptors expressed by pDCs are not functional, and other molecules are involved in the chemoattraction of these cells. We found increased expression of interleukin (IL)-18 in glomeruli of patients with active LN along with glomerular infiltration by pDCS. Since pDCs bear IL-18 receptor (IL-18R), it is conceivable that circulating pDCs may migrate toward glomeruli by IL-18/IL-18R interactions. Therefore, the relative depletion of circulating pDCs reflects the severity of inflammatory disease in LN.
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