CD4⁺ T cells are important drivers of tissue damage in immune-mediated renal diseases, such as anti-glomerular basement membrane glomerulonephritis, anti-neutrophil cytoplasmic antibody-associated glomerulonephritis, and lupus nephritis. The discovery of a distinct, IL-17-producing CD4⁺ T-cell lineage termed T helper type 17 (T_H17) cells has markedly advanced current understanding of the pathogenic mechanisms of organ-specific immunity and the pathways that lead to target organ damage. T_H17 cells are characterized by the expression of the transcription factor RORγt, the production of the pro-inflammatory cytokines IL-17A, IL-17F, IL-22, and high expression of the chemokine receptor C-C-motif chemokine receptor 6 (CCR6). An emerging body of evidence from experimental models and human studies supports a key role for these cells in the development of renal damage, and has led to the identification of targets to inhibit the production of T_H17 cells in the intestine, their migration, or their actions within the kidney. Here, we describe the identification, regulation, and function of T_H17 cells and their associated pathways in immune-mediated kidney diseases, with a particular focus on the mechanisms underlying renal tissue injury. We also discuss the rationale for the translation of these findings into new therapeutic approaches in patients with autoimmune kidney disease.

中文翻译：

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免疫介导的肾小球疾病中的T辅助型17细胞

CD4 ⁺ T细胞是免疫介导的肾脏疾病，例如抗肾小球基底膜肾小球肾炎，抗中性粒细胞胞浆抗体相关性肾小球肾炎和狼疮肾炎的重要组织损伤驱动器。发现了一种独特的，产生IL-17的CD4 ⁺ T细胞谱系，称为T辅助型17（T _H 17）细胞，目前已对器官特异性免疫的致病机制和导致靶器官的途径有了明显的了解。损害。Ť _ħ 17细胞的特征在于所述转录因子ROR的表达γt，促炎细胞因子IL-17A，IL-17F，IL-22的产生和趋化因子受体CC-基序趋化因子受体6（CCR6）的高表达。来自实验模型和人体研究的大量证据支持这些细胞在肾损伤发展中的关键作用，并导致鉴定出抑制肠中T _H 17细胞产生，抑制其迁移或迁移的靶标。它们在肾脏内的作用。在这里，我们描述T _H的识别，调控和功能免疫介导的肾脏疾病中的17种细胞及其相关途径，特别关注肾脏组织损伤的潜在机制。我们还讨论了将这些发现转化为自身免疫性肾脏疾病患者的新治疗方法的基本原理。