Tissue-specific therapy in immune-mediated kidney diseases: new ARGuments for targeting the IL-23/IL-17 axis
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Tissue-specific therapy in immune-mediated kidney diseases: new ARGuments for targeting the IL-23/IL-17 axis. / Krebs, Christian F; Turner, Jan-Eric; Riedel, Jan-Hendrik; Panzer, Ulf.
In: J CLIN INVEST, Vol. 131, No. 12, e150588, 15.06.2021.Research output: SCORING: Contribution to journal › Other (editorial matter etc.) › Research
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TY - JOUR
T1 - Tissue-specific therapy in immune-mediated kidney diseases: new ARGuments for targeting the IL-23/IL-17 axis
AU - Krebs, Christian F
AU - Turner, Jan-Eric
AU - Riedel, Jan-Hendrik
AU - Panzer, Ulf
PY - 2021/6/15
Y1 - 2021/6/15
N2 - 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.
AB - 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.
U2 - 10.1172/JCI150588
DO - 10.1172/JCI150588
M3 - Other (editorial matter etc.)
C2 - 34128472
VL - 131
JO - J CLIN INVEST
JF - J CLIN INVEST
SN - 0021-9738
IS - 12
M1 - e150588
ER -
