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Kidney transplantation is the preferred therapy for kidney failure. The leading cause of graft loss is chronic al- lograft nephropathy (CAN). We hypothesize that Interleukin-13 (IL-13), protective against acute kidney graft rejection, is involved in CAN. In mouse kidney allografts, we observe after 2 weeks signs of interstitial inflammation progressing to vasculitis. By 6 weeks, CAN is manifest. IL-13 is overexpressed in allografts versus isografts (p<0.01) throughout the post-transplant course. Concomitantly, we detect markers of fibrogenesis and epithelial-mesenchymal transition. To ex- plore this phenomenon, kidney proximal tubular epithelial cells were cultured with IL-13. Within 6 hours, we show in- creased proliferation compared to untreated cells (p<0.01), occurring through activation of IL4R /JAK3 and Stat6 and blocked by anti-IL-13 monoclonal antibody. This is the first report of IL-13 inducing a specific biological activity in kid- ney epithelial cells with a possible role in the damage control machinery, indicating its potential as a biomarker and thera- peutic target.

Interleukin-13 is Expressed in Mouse Kidney Allograft Rejection and Mediates Proliferation of Renal Tubular Epithelium In Vitro