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|Title:||A role for regulatory T cells in renal acute kidney injury|
|Authors:||Monteiro, Rebecca M. M. [UNIFESP]|
Camara, Niels O. S. [UNIFESP]
Rodrigues, Mauricio M. [UNIFESP]
Tzelepis, Fanny [UNIFESP]
Damiao, Marcio J. [UNIFESP]
Cenedeze, Marcos A. [UNIFESP]
Teixeira, Vicente de Paula A.
Reis, Marlene A. dos
Pacheco-Silva, Alvaro [UNIFESP]
Universidade de São Paulo (USP)
Universidade Federal de São Paulo (UNIFESP)
Hosp Albert Einstein
|Keywords:||Acute renal failure|
Ischemia and reperfusion injury
|Citation:||Transplant Immunology. Amsterdam: Elsevier B.V., v. 21, n. 1, p. 50-55, 2009.|
|Abstract:||Ischemia reperfusion injury (IRI) is a potential contributor for the development of chronic allograft nephropathy. T cells are important mediators of injury, even in the absence of alloantigens. We performed a depletion of TCD4(+)CTLA4(+)Foxp3(+) cells with anti-CD25(PC61), a treatment with anti-GITR (DTA-1) and rat-IgG, followed by 45 min of ischemia and 24/72 h of reperfusion, and then analyzed blood urea, kidney histopathology and gene expression in kidneys by QReal Time PCR. After 24 h of reperfusion, depletion of TCD4(+)CTLA4(+)Foxp3(+) cells reached 30.3%(spleen) and 67.8%(lymph nodes). 72 h after reperfusion depletion reached 43.1%(spleen) and 90.22%(lymph nodes) and depleted animals presented with significantly poorer renal function, while DTA-1 (anti-GITR)-treated ones showed a significant protection, all compared to serum urea from control group (IgG: 150.10 +/- 50.04; PC61: 187.23 +/- 31.38; DTA-1: 64.53 +/- 25.65, mg/dL, p<0.05). These data were corroborated by histopathology. We observed an increase of HO-1 expression in animals treated with DTA-1 at 72 h of reperfusion with significant differences. Thus, our results suggest that PC61 (anti-CD25) mAb treatment is deleterious, while DTA-1 (anti-GITR) mAb treatment presents a protective role in the renal IRI, indicating that some regulatory populations of T cells might have a role in IRI. (C) 2009 Elsevier B.V. All rights reserved.|
|Appears in Collections:||Artigo|
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