Affiliations 

  • 1 Department of Medical Microbiology and Clinical Microbiology, Faculty of Medicine, Near East University, Nicosia, Cyprus
  • 2 Department of Infectious Diseases and Clinical Microbiology, Hitit University Erol Olcok Corum Training and Research Hospital, Corum, Turkey
  • 3 Department of Medical Microbiology, Faculty of Medicine, Hitit University, Corum, Turkey
  • 4 Department of Biostatistics, Faculty of Medicine, Near East University, Nicosia, Cyprus
  • 5 Department of Nutrition and Dietetics, Faculty of Health Science, Hitit University, Corum, Turkey
  • 6 Department of Medical Microbiology, Faculty of Medicine, TOBB University of Economics and Technology; Ankara, Turkey
Trop Biomed, 2022 Dec 01;39(4):587-591.
PMID: 36602220 DOI: 10.47665/tb.39.4.016

Abstract

Crimean-Congo haemorrhagic fever (CCHF) is a severe human infection which can lead to fatal consequences. Acute CCHF patients were previously shown to exhibit frequencies of regulatory T-cell (Treg) but lower Treg-mediated suppressive activities than the healthy counterparts. This study aims is to investigate the phosphorylation levels of Foxp3 protein (master regulator of Treg cells) in CCHF patients. Blood samples collected from 18 CCHF patients and nine healthy volunteers were used to isolate peripheral blood mononuclear cells (PBMCs). Total and phosphorylated Foxp3 expression levels in the isolated PBMC samples were monitored by western blot and quantified using ImageJ software. Total Foxp3 expression levels in CCHF patients displayed decreasing trend, but not significantly. In contrast, significantly lower expression levels of phosphorylated Foxp3 were reported in CCHF patients. Our results suggest a possible association between Foxp3 dephosphorylation and CCHF pathogenesis. Nevertheless, more studies are required to evaluate the effect of Foxp3 dephosphorylation on Treg function, which would not only help to enlighten the CCHF pathogenesis but also contribute to the development of effective treatment strategies.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.