Emerging roles of the Th17/IL-17-axis in glomerulonephritis

Ramani, Kritika; Biswas, Partha S.

doi:10.1016/j.cyto.2015.07.029

Cited by 15 publications

(16 citation statements)

References 94 publications

(100 reference statements)

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“…It is well known that Th17 cells are involved in the regulation of LN pathogenesis through multiple mechanisms19. Th17 cells are a major type of pro-inflammatory T cells and many cytokines and transcription factors mediate the pathways that drive Th17 cell differentiation and promote Th17 immune responses32.…”

Section: Discussionmentioning

confidence: 99%

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Nuclear Factor Erythroid 2-related Factor 2 Deficiency Exacerbates Lupus Nephritis in B6/lpr mice by Regulating Th17 Cell Function

Zhao

Chen

Ding

et al. 2016

Sci Rep

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Lupus nephritis (LN) is the major clinical manifestation of systemic lupus erythematosus. LN is promoted by T helper 17 (Th17) cells, which are the major pro-inflammatory T cell subset contributing to autoimmunity regulation. Nuclear factor erythroid 2-related factor 2 (NRF2) is critical for suppressing reactive oxygen species (ROS) and relieving oxidant stress by regulating antioxidant gene expression. Previous studies have demonstrated that Nrf2 deficiency promotes drug-induced or spontaneous LN. However, whether NRF2 regulates Th17 function during LN development is still unclear. In this study, we introduced Nrf2 deficiency into a well-known LN model, the B6/lpr mouse strain, and found that it promoted early-stage LN with altered Th17 activation. Th17 cells and their relevant cytokines were dramatically increased in these double-mutant mice. We also demonstrated that naïve T cells from the double-mutant mice showed significantly increased differentiation into Th17 cells in vitro, with decreased expression of the Th17 differentiation suppressor Socs3 and increased phosphorylation of STAT3. Our results demonstrated that Nrf2 deficiency promoted Th17 differentiation and function during LN development. Moreover, our results suggested that the regulation of Th17 differentiation via NRF2 could be a therapeutic target for the treatment of subclinical LN patients.

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Section: Discussionmentioning

confidence: 99%

“…Th17 also co-regulates the pathogenesis of SLE together with type I interferon15, which regulates the germinal centre reactions by IL-21- and IL-17-dependent follicular Th cells in BXD2 mice161718. It is well known that Th17 cells regulate SLE pathogenesis through multiple mechanisms19.…”

mentioning

confidence: 99%

Nuclear Factor Erythroid 2-related Factor 2 Deficiency Exacerbates Lupus Nephritis in B6/lpr mice by Regulating Th17 Cell Function

Zhao

Chen

Ding

et al. 2016

Sci Rep

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“…IL‐17A is a proinflammatory cytokine involved in kidney disease . In vitro, IL‐17A promotes podocyte apoptosis and downregulates phosphor‐nephrin levels in podocytes .…”

Section: Discussionmentioning

confidence: 99%

“…Studies show that the Th17/IL‐17A axis plays an important role in the pathogenesis of chronic kidney disease (CKD) . IL‐17A is a crucial proinflammatory cytokine that acts as an important node connecting the innate and adaptive immune systems.…”

Section: Introductionmentioning

confidence: 99%

“…Studies show that the Th17/IL-17A axis plays an important role in the pathogenesis of chronic kidney disease (CKD). [1][2][3] IL-17A is a crucial proinflammatory cytokine that acts as an important node connecting the innate and adaptive immune systems. It recruits neutrophils to the kidney and contributes to the formation of an inflammatory milieu by stimulating mesangial cells and tubular epithelial cells to secrete chemokines and other proinflammatory mediators.…”

Section: Introductionmentioning

confidence: 99%

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Interleukin‐17A participates in podocyte injury by inducing IL‐1β secretion through ROS‐NLRP3 inflammasome‐caspase‐1 pathway

Yan

Yang

et al. 2018

Scand J Immunol

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Studies show that the Th17/IL-17A axis plays an important role in the pathogenesis of kidney diseases. Previously, we also showed that IL-17A may play a role in the pathogenesis of primary nephrotic syndrome; however, the underlying mechanism(s) is unclear. The aim of this study was to explore the molecular mechanism of IL-17A-inducing podocyte injury in vitro. In this study, the NLRP3 inflammasome activation and the morphology of podocytes were detected by Western blot and immunofluorescence. The results showed that podocytes persistently expressed IL-17A receptor and that NLRP3 inflammasome in these cells was activated upon exposure to IL-17A. Also, activity of caspase-1 and secretion of IL-1β increased in the presence of IL-17A. In addition, IL-17A disrupted podocyte morphology by decreasing expression of podocin and increasing expression of desmin. Blockade of intracellular ROS or inhibition of caspase-1 prevented activation of the NLRP3 inflammasome, thereby restoring podocyte morphology. Taken together, the results suggest that IL-17A induces podocyte injury by activating the NLRP3 inflammasome and IL-1β secretion and contributes to disruption of the kidney's filtration system.

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A new era in the treatment of kidney diseases: NLRP3 inflammasome and cytokine-targeted therapies

Leventoğlu,

Bakkaloğlu

2024

Pediatr Nephrol

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Emerging roles of the Th17/IL-17-axis in glomerulonephritis

Cited by 15 publications

References 94 publications

Nuclear Factor Erythroid 2-related Factor 2 Deficiency Exacerbates Lupus Nephritis in B6/lpr mice by Regulating Th17 Cell Function

Nuclear Factor Erythroid 2-related Factor 2 Deficiency Exacerbates Lupus Nephritis in B6/lpr mice by Regulating Th17 Cell Function

Interleukin‐17A participates in podocyte injury by inducing IL‐1β secretion through ROS‐NLRP3 inflammasome‐caspase‐1 pathway

A new era in the treatment of kidney diseases: NLRP3 inflammasome and cytokine-targeted therapies

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