Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/60040
Type: Artigo de periódico
Title: Increased Th1 activity in patients with coronary artery disease
Author: Fernandes, JL
Mamoni, RL
Orford, JL
Garcia, C
Selwyn, AP
Coelho, OR
Blotta, MHSL
Abstract: Background: Atherosclerotic lesions Lire mainly composed of macrophages and T lymphocytes. Specific T helper type I (Th1) cytokines and interferon gamma (IFN-gamma) inducible chemokines have been shown to be present in these lesions, modulating the local immunologic response. To explore whether this increase in Th1 activity could also be detected in circulating cells indicating a systemic activation, we studied the peripheral expression of Th I cytokines and chemokines in patients with coronary artery disease and controls. Methods and results: Fifty patients with coronary artery disease (25 with unstable angina and 25 with stable angina) and 10 controls were studied. Serum interleukin (IL)-12 and IFN-gamma and the expression of IFN-gamma inducible chemokines IP-10, Mig and their receptor CXCR3 in peripheral cells were analyzed. Serum IL-12 and intracellular expression of IFN-gamma were significantly elevated in patients with unstable angina. An enhanced expression of IFN-gamma chemokines IP-10, Mig and CXCR3 in patients with stable angina was also observed. Conclusions: This study demonstrates an increased systemic inflammatory activity in patients with coronary heart disease with a predominant Th1 response, particularly in patients with unstable angina, suggesting an important role played by this polarization in plaque formation and rupture. (C) 2004 Elsevier Ltd. All rights reserved.
Subject: atherosclerosis
coronary artery disease
inflammation
interleukins
Country: Inglaterra
Editor: Academic Press Ltd Elsevier Science Ltd
Rights: fechado
Identifier DOI: 10.1016/j.cyto.2004.01.007
Date Issue: 2004
Appears in Collections:Unicamp - Artigos e Outros Documentos

Files in This Item:
File Description SizeFormat 
WOS000221898200006.pdf178.1 kBAdobe PDFView/Open


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.