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Foxp3, Rorγt and Il-10 Cytokine Profile in Chronic Heart Failure Publisher Pubmed



Gorzin F1 ; Amirzargar AA1 ; Mahmoudi MJ2 ; Rahnemoon Z3 ; Najmi Varzaneh F4, 5 ; Hedayat M6, 7 ; Sadati S1 ; Eskandari V1 ; Rahmati Z1 ; Rezaei N1, 8, 9
Authors
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Authors Affiliations
  1. 1. Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  2. 2. Department of Cardiology, Amir Alam Hospital, Tehran University of Medical Sciences, Tehran, Iran
  3. 3. Cardiac Heart Center, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  4. 4. The Russell H. Morgan Department of Radiology and Radiological Sciences, Johns Hopkins University School of Medicine, Baltimore, MD, United States
  5. 5. Network of Immunity in Infection, Malignancy and Autoimmunity (NIIMA), Universal Scientific Education and Research Network (USERN), Baltimore, MD, United States
  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. Research Center for Immunodeficiencies, Pediatrics Center of Excellence, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran
  9. 9. Network of Immunity in Infection, Malignancy and Autoimmunity (NIIMA), Universal Scientific Education and Research Network (USERN), Sheffield, United Kingdom

Source: Bratislava Medical Journal Published:2017


Abstract

BACKGROUND: Distinct subsets of T cells play crucial regulatory roles in inflammatory processes of chronic heart failure (CHF). Retinoic acid receptor-related orphan receptor-γt (Ror-γt) and Forkhead box P3 (Foxp3) have been defined as the master regulators of Th17 cells and Treg cells, respectively. At the same time, antiinflammatory cytokines such as IL-10 may neutralize inflammation in CHF. The current study was designed to compare FOXP3, RORγt and IL-10 protein expression in the blood and IL-10 in supernatant PBMCs in CHF patients versus normal subjects. PATIENTS AND METHODS: Our study population consisted of 42 patients with CHF in four different function classes and 42 healthy subjects who served as controls. RNA extraction and cDNA synthesis was performed and mRNA expression for genes FOXP3, RORγt, IL-10 was determined by RT-PCR. The amount of IL-10 protein in supernatant of PBMCs was measured by ELISA technique. RESULTS: There was no significant difference in FOXP3, RORγt, IL-10 protein expression and supernatant PBMCs IL-10 in CHF patients as compared to control. The level of Foxp3 was significantly lower in CHF patients with ischemic vs non-ischemic cause (p = 0.04). DISCUSSION: Although inflammation plays a central role in the pathophysiology of CHF, the roles of FOXp3, RORγt, and IL-10 remain to be determined.