Izvorni znanstveni članak
https://doi.org/10.3325/cmj.2018.59.139
Association of levels of interleukin 17 and T-helper 17 count with symptom severity and etiology of chronic heart failure: a case-control study
Zahra Rahmati
; Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
Ali Akbar Amirzargar
; Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
Samaneh Saadati
; Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
Farzaneh Rahmani
; Research Center for Immunodeficiencies, Pediatrics Center of Excellence, Children’s Medical Center Tehran University of Medical Sciences, Tehran, Iran
Mohammad Jafar Mahmoudi
; Department of Cardiology, Amir Alam Hospital, Tehran University of Medical Sciences, Tehran, Iran
Zahra Rahnemoon
; Department of Cardiology, Amir Alam Hospital, Tehran University of Medical Sciences, Tehran, Iran
Vajiheh Eskandari
; Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
Fatemeh Gorzin
; Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
Mona Hedayat
; Division of Immunology, Boston Children’s Hospital, Harvard Medical School, Boston, MA, USA
Nima Rezaei
; Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
Sažetak
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.
Ključne riječi
Hrčak ID:
237476
URI
Datum izdavanja:
15.8.2018.
Posjeta: 741 *