Tissue-specific therapy in immune-mediated kidney diseases: new ARGuments for targeting the IL-23/IL-17 axis

J Clin Invest. 2021 Jun 15;131(12):e150588. doi: 10.1172/JCI150588.


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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Comment

MeSH terms

  • Cytokines
  • Humans
  • Interleukin-17* / genetics
  • Interleukin-23
  • Kidney
  • Kidney Diseases* / drug therapy
  • Kidney Diseases* / genetics


  • Cytokines
  • Interleukin-17
  • Interleukin-23