III. Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
III. Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany; Section of Translational Immunology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Mol Immunol. 2018 Dec;104:90-99. doi: 10.1016/j.molimm.2018.09.005. Epub 2018 Nov 15.
Immune-mediated glomerular diseases (glomerulonephritis) encompass a heterogeneous collection of diseases that cause inflammation within the glomerulus and other renal compartments with significant morbidity and mortality. In general, CD4 T cells orchestrate the immune response and play a unique role in autoimmune and chronic inflammatory diseases. In particular, the characterization of a distinct, IL-17 cytokines producing CD4 T cell subset named T17 cells has significantly advanced the current understanding of the pathogenic mechanisms of organ-specific immunity. Our group and others have shown that the recruitment of T17 cells to the inflamed kidney drives renal tissue injury in experimental and possibly human crescentic glomerulonephritis (GN), but much remains to be understood about the biological functions, regulation, and signaling pathways of the T17/IL-17 axis leading to organ damage. Here we review our current knowledge about the mechanisms and functions of IL-17 signaling in renal autoimmune diseases, with a special focus on experimental and human crescentic GN.
免疫介导的肾小球疾病(肾小球肾炎)包括一组异质性疾病,这些疾病会导致肾小球和其他肾脏部位发生炎症,具有显著的发病率和死亡率。一般来说,CD4 T 细胞协调免疫反应,并在自身免疫和慢性炎症性疾病中发挥独特作用。特别是,一种独特的、产生白细胞介素-17(IL-17)细胞因子的 CD4 T 细胞亚群的特征,即 T17 细胞,极大地促进了对器官特异性免疫的发病机制的现有理解。我们的小组和其他小组已经表明,T17 细胞向炎症肾脏的募集会导致实验性和可能的人类新月体肾小球肾炎(GN)中的肾脏组织损伤,但对于 T17/IL-17 轴导致器官损伤的生物学功能、调节和信号通路,仍有许多需要了解。在这里,我们回顾了关于 IL-17 信号在肾脏自身免疫性疾病中的机制和功能的现有知识,特别关注实验性和人类新月体 GN。