Fig. 1.
Experimental schema of studies carried out to investigate the role of T cells in chronic kidney disease (CKD) progression following acute kidney injury (AKI). Renal injury was induced by unilateral ischemia-reperfusion (I/R) injury to the left kidney by clamping the renal pedicle for 40 min (red circle). The rats were allowed to recover for 33 days on a standard diet containing 0.4% NaCl. To hasten CKD, rats were subjected to unilateral nephrectomy (UNx) at day 33 postsurgery (red X) and subsequently placed on high-salt diet (4% NaCl). Sham-operated rats received similar treatment without clamping on day 0 but also with UNx at day 33. A: study I investigated the effect of T cell inhibition in the AKI-CKD transition. Rats from both genotypes were treated from day 35 to day 63 with either mycophenolate mofetil (MMF, 30 mg·kg−1·day−1) or vehicle (sugar-free chocolate pudding at 1 g/kg) daily. B: study II was designed to identify the source of I/R-induced IL-17 production, with cohorts sacrificed 2 or 35 days postsurgery. C: study III was designed to investigate the effect of IL-17 antagonism by administration of IL-17Rc along with high-salt diet.