The role of interleukin-17A in the pathogenesis of kidney diseases

被引:98
作者
Cortvrindt, Charlotte [1 ]
Speeckaert, Reinhart [2 ]
Moerman, Alena [3 ]
Delanghe, Joris R. [3 ]
Speeckaert, Marijn M. [1 ]
机构
[1] Ghent Univ Hosp, Dept Nephrol, De Pintelaan 185, B-9000 Ghent, Belgium
[2] Ghent Univ Hosp, Dept Dermatol, Ghent, Belgium
[3] Ghent Univ Hosp, Dept Clin Chem, Ghent, Belgium
关键词
Interleukin-17A; inflammation; kidney disease; T-HELPER; 17; GAMMA-DELTA T; TH17; CELLS; GENE POLYMORPHISMS; IL-17; EXPRESSION; LUPUS NEPHRITIS; ACUTE REJECTION; RENAL INJURY; TRANSPLANT RECIPIENTS; EPITHELIAL-CELLS;
D O I
10.1016/j.pathol.2017.01.003
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
Being a member of the IL-17 family, comprising six structurally related ligands, IL-17A is a cytokine, produced by multiple cell types, such as CD4(+) ab T cells, gamma delta T cells, natural killer cells, neutrophils, macrophages, dendritic cells, lymphoid tissue inducer cells, mast cells and plasma cells. IL-17A participates in tissue inflammation by inducing the expression of chemokines, proinflammatory cytokines and matrix metalloproteases. Besides its role in host defence against infectious diseases, IL-17A is involved in different autoimmune and inflammatory diseases. In this review, we will highlight the role of IL-17A in the pathogenesis of acute and chronic kidney diseases. Due to its pleiotropic character, IL-17A is involved in the development of atherosclerosis, hypertension, diabetic nephropathy, ischaemia-reperfusion injury, fibrosis, glomerulonephritis, nephrotic syndrome, minimal change disease and acute renal allograft rejection. In addition, inhibition of IL-17A may be a promising therapeutic target to prevent end-stage renal disease.
引用
收藏
页码:247 / 258
页数:12
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