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Acute kidney injury (AKI) is a frequent event associated with decreased allograft survival in patients with transplanted kidneys and high mortality in patients with native kidneys (1,2). AKI is a common complication in hospitalized patients, and its incidence has risen substantially over the past 15 years (1-3). As a conservative estimate, roughly 17 million admissions annually in the United States are complicated by AKI, resulting in over $10 billion in costs to the health care system (4). Kidney transplants from living unrelated donors (not well HLA matched) with minimal ischemic injury have improved allograft survival, compared with grafts from well matched cadaveric donors with significant ischemia (5, 6). This implies that renal ischemia reperfusion injury (IRI) can have important consequences on long-term graft survival and native kidneys. IRI is a highly complex cascade of events that includes interactions between vascular endothelium, interstitial compartments, circulating cells, and numerous mediator molecules (7). Renal ischemic injury has been found to permanently damage peritubular capillaries causing hypoxia, which may be involved in the progression of chronic renal disease after AKI (7, 8). Tubulointerstitial influx of inflammatory cells is found in many forms of chronic renal diseases, including ‘nonimmune’ diseases such as diabetes and hypertension (9). Tlymphocyte infiltration has also been observed early after moderate ischemia injury (10,11) however, the dynamics of infiltrating lymphocyte populations long term after moderate or severe ischemic injury is not very clear. It has been demonstrated that T and B lymphocytes are important mediators in the pathogenesis of renal IRI (10, 12) however, the mechanisms by which these cells induce kidney injury is largely unknown. The trafficking of pathogenic lymphocytes into kidneys after moderate and severe ischemic injury has been postulated to contribute to kidney damage (11, 13, 14) however the physiologic state and the dynamics of trafficking of these populations long term after ischemia have not been rigorously studied. Furthermore, the activation and expression of the effector-memory phenotype by infiltrated lymphocytes suggests the possibility that these lymphocytes are responding to an injury-associated antigen (15, 16). In addition, these lymphocytes are responsible to produce inflammatory mediators not only causing local kidney structure damage, but also the severe effects

Mechanisms of T Lymphocytes in the Damage and Repair Long Term after Renal Ischemia Reperfusion Injury