IL-17 mediates neutrophil infiltration and renal fibrosis following recovery from ischemia reperfusion:compensatory role of Natural Killer cells in athymic rats.

IL-17 mediates neutrophil infiltration and renal fibrosis following recovery from ischemia reperfusion:compensatory role of Natural Killer cells in athymic rats. Am J Physiol Renal Physiol. 2016 Nov 16;:ajprenal.00462.2016 Authors: Mehrotra P, Collett JA, McKinney S, Stevens J, Ivancic CM, Basile DP Abstract T cells have been implicated in the pathogenesis of AKI as well as its progression to CKD. Previous studies suggest that Th17 cells participates during the AKI to CKD transition and inhibition of T cell activity by mycophenolate mofetil (MMF) or losartan attenuates the development of fibrosis following AKI. We hypothesized that T cell deficient rats may have reduced levels of IL-17 cytokine leading to decreased fibrosis following AKI. Renal I/R was performed on T cell deficient athymic rats (Foxn1rnu-/rnu-) and control euthymic rats (Foxn1rnu-/+) and CKD progression was hastened by unilateral nephrectomy at Day 33 and subsequent exposure to 4.0% sodium diet. Renal fibrosis developed in euthymic rats and was reduced by MMF treatment. Athymic rats exhibited a similar degree of fibrosis but this was unaffected by MMF treatment. FACS analysis demonstrated that the number of IL-17+ cells was similar between post ischemic athymic vs euthymic rats. The source of IL-17 production in euthymic rats was predominately from conventional T cells (CD3+/CD161-). In the absence of conventional T-cells in athymic rats, a compensatory pathway invol...
Source: Am J Physiol Renal P... - Category: Urology & Nephrology Authors: Tags: Am J Physiol Renal Physiol Source Type: research