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Association of Levels of Interleukin 17 and T-Helper 17 Count With Symptom Severity and Etiology of Chronic Heart Failure: A Case-Control Study Publisher Pubmed



Rahmati Z1 ; Amirzargar AA1, 2 ; Saadati S1 ; Rahmani F3, 4 ; Mahmoudi MJ5 ; Rahnemoon Z5 ; Eskandari V1 ; Gorzin F1 ; Hedayat M6, 7 ; Rezaei N1, 2, 3, 8
Authors
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Authors Affiliations
  1. 1. Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Poursina Avenue, Tehran, Iran
  2. 2. Molecular Immunology Research Center, Tehran University of Medical Sciences, Tehran, Iran
  3. 3. Research Center for Immunodeficiencies, Pediatrics Center of Excellence, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran
  4. 4. NeuroImaging Network (NIN), Universal Scientific Education and Research Network (USERN), Tehran, Iran
  5. 5. Department of Cardiology, Amir Alam Hospital, Tehran University of Medical Sciences, Tehran, Iran
  6. 6. Division of Immunology, Boston Children's Hospital, Harvard Medical School, Boston, MA, United States
  7. 7. Network of Immunity in Infection, Malignancy and Autoimmunity (NIIMA), Universal Scientific Education and Research Network (USERN), Boston, MA, United States
  8. 8. Network of Immunity in Infection, Malignancy and Autoimmunity (NIIMA), Universal Scientific Education and Research Network (USERN), Tehran, Iran

Source: Croatian Medical Journal Published:2018


Abstract

Aim: To assess the association between the levels of interleukin 17 (IL-17) and T-helper 17 count and symptom severity and etiology of chronic heart failure. Methods: This single-center prospective case-control study, conducted from December 1, 2015 to January 1, 2017 in Tehran Heart Center, evaluated gene expression of IL-17, relative count of (CD4+IL17+) Th17 cells and CD4+ helper T-cells in peripheral blood mononuclear cells of 42 patients with CHF and 42 matched controls. A multiple regression model assessed the predictors of peripheral IL-17 expression and Th17 count in patients with CHF. Results: IL-17 expression was increased in patients with CHF, both at baseline and after stimulation. IL-17 and Th17 counts were higher in patients with advanced New York Heart Association (NYHA) functional class (class IV) than in controls and patients with class I. Th17 cell population expanded in patients with CHF, more prominently in patients with class IV than in controls and patients with class I, regardless of the ischemic or non-ischemic CHF origin. Multiple regression model showed that NYHA was the only meaningful predictor of IL-17 levels and Th17 count. Conclusion: We demonstrated the lymphocytic origin of IL-17 production in advanced CHF and the ability of disease severity to predict IL-17 levels. © 2018 Medicinska Naklada Zagreb. All rights reserved.