Human AKI is manifested by inflammation, and an early feature in the pathogenesis is the accumulation of immune cells in the kidney. To understand the pathophysiology of AKI, results from animal models have shown a causal relation between the leukocyte activation and infiltration to the kidney after kidney ischemia-reperfusion. Blocking the activation or trafficking of proinflammatory leukocytes into the kidney preserves renal function and histologic integrity. In contrast, the anti-inflammatory lymphocytes called regulatory T cells have an intrinsic renal-protective function and may represent a novel therapeutic approach and/or target for pharmacological manipulation to ameliorate AKI. This review will highlight the recent insight gained into the role and mechanisms of regulatory T cells in AKI.