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The IL-23/Th17 Axis Contributes to Renal Injury in Experimental Glomerulonephritis
Open accessAbstract
T cells infiltrate the kidney in both human and experimental glomerulonephritis, and several lines of evidence indicate that T cell-mediated tissue damage plays an important role in the immunopathogenesis of renal inflammatory diseases. However, the functions of the different T cell subsets, particularly the recently identified interleukin-17 (IL-17)-producing T cells (Th17 cells), are incompletely understood in glomerulonephritis. Here, we identified renal IL-17-producing T cells in the T cell-mediated model of nephrotoxic nephritis in mice. In vitro, IL-17 enhanced the production of the proinflammatory chemokines CCL2/MCP-1, CCL3/MIP-1alpha, and CCL20/LARC, which are implicated in the recruitment of T cells and monocytes, in mouse mesangial cells. To determine the function of Th17 cells in renal inflammation, we induced nephrotoxic nephritis in IL-23 p19(-/-) mice, which have reduced numbers of Th17 cells, and in IL-17(-/-) mice, which are deficient in the effector cytokine IL-17 itself. In comparison with nephritic wild-type mice, IL-23 p19(-/-) mice demonstrated less infiltration of Th17 cells, and both IL-23 p19(-/-) and IL-17(-/-) mice developed less severe nephritis as measured by renal function, albuminuria, and frequency of glomerular crescent formation. These results demonstrate that the IL-23/IL-17 pathway significantly contributes to renal tissue injury in experimental glomerulonephritis. Targeting the IL-23/Th17 axis may be a promising therapeutic strategy for the treatment of proliferative and crescentic glomerulonephritis.
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A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17
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IL-23 drives a pathogenic T cell population that induces autoimmune inflammation
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IL-17 family cytokines and the expanding diversity of effector T cell lineages
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Divergent Pro- and Antiinflammatory Roles for IL-23 and IL-12 in Joint Autoimmune Inflammation
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Self-citationNF-κB in inflammation and renal diseases
Zhang, H., & Sun, S.-C. (2015) · Cell & Bioscience · doi:10.1186/s13578-015-0056-4 · Cited by 383
Immune and Inflammatory Role in Renal Disease
Imig, J. D., & Ryan, M. J. (2013) · Comprehensive Physiology · doi:10.1002/cphy.c120028 · Cited by 356
Bechara, R., Amatya, N., Bailey, R. D., Li, Y., Aggor, F. E. Y., Li, D.-D., Jawale, C. V., Coleman, B. M., Dai, N., Gokhale, N. S., et al. (2021) · Science Immunology · doi:10.1126/sciimmunol.abd1287 · Cited by 89
Moschovaki Filippidou, F., Kirsch, A. H., Thelen, M., Kétszeri, M., Artinger, K., Aringer, I., Schabhüttl, C., Mooslechner, A. A., Frauscher, B., Pollheimer, M., et al. (2020) · The American Journal of Pathology · doi:10.1016/j.ajpath.2019.10.008 · Cited by 66
Metadata
- Authors
- Paust, H.-J., Turner, J.-E., Steinmetz, O. M., Peters, A., Heymann, F., Ho[Combining Diaeresis]lscher, C., Wolf, G., Kurts, C., Mittru[Combining Diaeresis]cker, H.-W., Stahl, R. A. K., & Panzer, U.
- Venue
- Journal of the American Society of Nephrology
- Published
- 2009-05
- Volume
- 20
- Issue
- 5
- Pages
- 969-979
- ISSN
- 1046-6673 (ISSN-L)
- OpenAlex
- W2140920572
- Cited by
- 245
- References
- 8
- FWCI
- 11.34
- Type
- journal article
- Language
- en
- Open access
- green
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- Paust, H.-J., Turner, J.-E., Steinmetz, O. M., Peters, A., Heymann, F., Ho[Combining Diaeresis]lscher, C., Wolf, G., Kurts, C., Mittru[Combining Diaeresis]cker, H.-W., Stahl, R. A. K., & Panzer, U. (2009). The IL-23/Th17 Axis Contributes to Renal Injury in Experimental Glomerulonephritis. Journal of the American Society of Nephrology. https://doi.org/10.1681/asn.2008050556
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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