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      T Lymphocytes and Acute Kidney Injury: Update

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          The immune system is among the key pathogenic factors in acute kidney injury (AKI). Various immune cells, including dendritic cells, natural killer T cells, T and B lymphocytes, neutrophils and macrophages are involved. Conventional CD4+ lymphocytes are well established to participate in early injury, and CD4+CD25+FoxP3 regulatory T cells are protective and can accelerate repair. A newly identified kidney T cell receptor + CD4-CD8- (double-negative) T cell has complex functions, including potentially anti-inflammatory roles in AKI. In this mini review, we summarize the data on the role of lymphocytes in AKI and set the stage for further mechanistic studies as well as interventions to improve outcomes.

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          Most cited references 13

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          Expanded Double Negative T Cells in Patients with Systemic Lupus Erythematosus Produce IL-17 and Infiltrate the Kidneys

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            Regulatory T cells suppress innate immunity in kidney ischemia-reperfusion injury.

            Both innate and adaptive mechanisms participate in the pathogenesis of kidney ischemia-reperfusion injury (IRI), but the role of regulatory immune mechanisms is unknown. We hypothesized that the anti-inflammatory effects of CD4(+)CD25(+)FoxP3(+) regulatory T cells (Tregs) protect against renal IRI. Partial depletion of Tregs with an anti-CD25 mAb potentiated kidney damage induced by IRI. Reducing the number of Tregs resulted in more neutrophils, macrophages, and innate cytokine transcription in the kidney after IRI but did not affect CD4(+) T cells or B cells. We performed adoptive transfer of lymph node cells from wild-type mice or FoxP3-deficient Scurfy mice into T cell- and B cell-deficient RAG-1 knockout mice to generate mice with and without FoxP3(+) Tregs, respectively. FoxP3(+) Treg-deficient mice accumulated a greater number of inflammatory leukocytes after renal IRI than mice containing Tregs. To confirm that a lack of Tregs potentiated renal injury, we co-transferred isolated Tregs and Scurfy lymph node cells; Treg repletion significantly attenuated IRI-induced renal injury and leukocyte accumulation. Furthermore, although adoptive transfer of wild-type Tregs into RAG-1 knockout mice was sufficient to prevent kidney IRI, transfer of IL-10-deficient Tregs was not. Taken together, these results demonstrate that Tregs modulate injury after kidney IRI through IL-10-mediated suppression of the innate immune system.
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              Inflammatory cells in ischemic acute renal failure.

              Ischemic acute renal failure (ARF) is increasingly recognized as involving a complex cascade of mechanisms with both acute and chronic consequences. Attention to nontraditional mediators of ARF such as inflammatory pathways and microvascular events has yielded new paradigms and avenues of research. The initiation phase of renal ischemia/reperfusion (I/R) injury damage involves microvascular hemodynamic changes characterized by red blood cell sludging with platelets and leukocytes. Blocking leukocyte-endothelial interactions has yielded significant protection from renal I/R injury in experimental models. However, experiments focusing on the role of the neutrophil have led to a modest expectation of its role in ARF. Recent studies have found that T cells directly mediate renal injury in experimental I/R injury. The CD4+ T cell, working both via interferon-gamma (IFN-gamma) and costimulatory molecules appears to be an important modulator of ARF. The B cell has recently been implicated in ARF. Little is known about the role for the macrophage. Finally, resident kidney cells likely contribute to the inflammatory pathogenesis of I/R damage and protection/repair, but how, and to what extent they are involved is not known. New tools to modulate inflammatory cells, particularly mononuclear leukocytes, hold promise for clinical trials in ARF.

                Author and article information

                Nephron Clin Pract
                Nephron Clinical Practice
                S. Karger AG
                September 2014
                24 September 2014
                : 127
                : 1-4
                : 51-55
                Departments of aPathology and bMedicine, Johns Hopkins University, Baltimore, Md., USA
                Author notes
                *Hamid Rabb, MD, Division of Nephrology, Department of Medicine, Johns Hopkins University, Ross 965, 720 Rutland Avenue, Baltimore, MD 21205 (USA), E-Mail hrabb1@jhmi.edu
                363719 PMC5264523 Nephron Clin Pract 2014;127:51-55
                © 2014 S. Karger AG, Basel

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                Page count
                Figures: 1, Pages: 5
                Original Paper


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