Please use this identifier to cite or link to this item: http://repositorio.unifesp.br/handle/11600/31566
Title: Toll-like receptors-related genes in kidney transplant patients with chronic allograft nephropathy and acute rejection
Authors: Nogueira, Eliana
Ponciano, Viviane Campos
Naka, Erika L.
Marques, Georgia D. M.
Cenedeze, Marcos A.
Saraiva Camara, Niels Olsen
Pacheco-Silva, Alvaro [UNIFESP]
Universidade Federal de São Paulo (UNIFESP)
Universidade de São Paulo (USP)
Keywords: Macroarray
Chronic allograft nephropathy
Acute vascular rejection
Acute non-vascular rejection
Kidney transplant
Nephrectomy
Issue Date: 1-Jun-2009
Publisher: Elsevier B.V.
Citation: International Immunopharmacology. Amsterdam: Elsevier B.V., v. 9, n. 6, p. 673-676, 2009.
Abstract: Introduction: Toll-like receptors (TLR) comprehend an emerging family of receptors that recognize pathogen-associated molecular patterns and promote the activation of leukocytes. Surgical trauma and ischemia-reperfusion injury are likely to provide exposure to endogenous ligands for TLR in virtually all kidney transplant recipients.Methods: Macroarray (GEArray OHS-018.2 Series-Superarray) analyses of 128 genes involved in TLR signaling pathway were performed in nephrectomy samples of patients with chronic allograft nephropathy (CAN) and acute rejection (AR, vascular and non vascular). the analysis of each membrane was performed by GEArray Expression Analysis Suite 2.0.Results: Macroarray profile identified a gene expression signature that could discriminate CAN and AR. Three genes were significantly expressed between CAN and vascular AR: Pellino 2; IL 8 and UBE2V1. in relation to vascular and non-vascular AR, there were only two genes with statistical significance: IL-6 and IRAK-3.Conclusion: Vascular and non-vascular AR and CAN showed different expression of a few genes in TLR pathway. the analysis of nephrectomy showed that activation of TLR pathway is present in AR and CAN. (C) 2008 Elsevier B.V. All rights reserved.
URI: http://repositorio.unifesp.br/handle/11600/31566
ISSN: 1567-5769
Other Identifiers: http://dx.doi.org/10.1016/j.intimp.2008.11.018
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