IL-17A is a novel player in dialysis-induced peritoneal damage.

Kidney international (2014-02-21)
Raquel Rodrigues-Díez, Luiz S Aroeira, Macarena Orejudo, M-Auxiliadora Bajo, José Jiménez Heffernan, Raúl R Rodrigues-Díez, Sandra Rayego-Mateos, Alberto Ortiz, Guadalupe Gonzalez-Mateo, Manuel López-Cabrera, Rafael Selgas, Jesús Egido, Marta Ruiz-Ortega

The classical view of the immune system has changed by the discovery of novel T-helper (Th) subsets, including Th17 (IL-17A-producing cells). IL-17A participates in immune-mediated glomerulonephritis and more recently in inflammatory pathologies, including experimental renal injury. Peritoneal dialysis patients present chronic inflammation and Th1/Th2 imbalance, but the role of the Th17 response in peritoneal membrane damage has not been investigated. In peritoneal biopsies from dialyzed patients, IL-17A immunostaining was found mainly in inflammatory areas and was absent in the healthy peritoneum. IL-17A-expressing cells included lymphocytes (CD4+ and γδ), neutrophils, and mast cells. Elevated IL-17A effluent concentrations were found in long-term peritoneal dialysis patients. Studies in mice showed that repeated exposure to recombinant IL-17A caused peritoneal inflammation and fibrosis. Moreover, chronic exposure to dialysis fluids resulted in a peritoneal Th17 response, including elevated IL-17A gene and protein production, submesothelial cell infiltration of IL-17A-expressing cells, and upregulation of Th17 differentiation factors and cytokines. IL-17A neutralization diminished experimental peritoneal inflammation and fibrosis caused by chronic exposure to dialysis fluids in mice. Thus, IL-17A is a key player of peritoneum damage and it may be a good candidate for therapeutic intervention in peritoneal dialysis patients.

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Anti-Fibronectin Antibody, Chemicon®, from rabbit