ArticleThe Journal of clinical investigation2021
Tissue-specific therapy in immune-mediated kidney diseases: new ARGuments for targeting the IL-23/IL-17 axis.
Article in The Journal of clinical investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 8 citations in OpenAlex.
- Sex-specific signatures of gut microbiota and systemic inflammation in patients with urolithiasis: a cross-sectional study.Frontiers in cellular and infection microbiology · 2026Article
- The immunoregulatory roles of non-haematopoietic cells in the kidney.Nature reviews. Nephrology · 2024Review
- Article
- Th17 cell plasticity towards a T-bet-dependent Th1 phenotype is required for bacterial control in Staphylococcus aureus infection.PLoS pathogens · 2022Article
- Clustering Inflammatory Markers with Sociodemographic and Clinical Characteristics of Patients with Diabetes Type 2 Can Support Family Physicians' Clinical Reasoning by Reducing Patients' Complexity.Healthcare (Basel, Switzerland) · 2021Article
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4 authors at 1 institution in 1 country.
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Abstract
Immune-mediated kidney diseases are a leading cause of end-stage renal disease. Despite recent discoveries, the immunopathogenesis of this heterogeneous disease group remains incompletely understood, which is a major reason for the lack of specific therapies and targeted interventions. Accumulating evidence suggests that cytokines related to the T cell response play an important role in renal autoimmunity. In this issue of the JCI, Li et al. demonstrate that IL-23 directly regulates the metabolism of parenchymal kidney cells, thereby generating a proinflammatory microenvironment that exacerbates T cell-driven renal tissue damage. These findings identify the IL-23/IL-17 axis as a key mediator of renal tissue injury and open new avenues for the development of pathogenesis-based treatment strategies in renal inflammatory diseases.
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