Document Type : Original Article
Authors
1 Department of Immunology & Microbiology, School of Medicine, Arak University of Medical Sciences, Arak, Iran
2 Molecular and Medicine Research Center, Arak University of Medical Sciences, Arak, Iran
3 Infectious Diseases Research Center (IDRC), Arak University of Medical Sciences, Arak, Iran
Abstract
Background and Aims Since in patients with type 2 diabetes (T2DM), there is an imbalance of inflammatory cells, the presence of inflammatory cytokines and defects in homeostasis are possible. The present study aimed to evaluate the percentage of Treg cells, lymphocytes, T cells, and T helper cells and gene expression of TGF-β cytokine in the T2DM patients.
Methods Fifty patients with T2DM and 50 healthy controls were included in this study, according to the inclusion criteria. The percentage of Treg cells, T cells, and T helper cells was determined by flow cytometry. Also, the expression of CD4, CD25, and FOXP3 markers of Treg cells was examined. The gene expression of TGF-β cytokine was evaluated by real-time polymerase chain reaction (PCR).
Results The percentage of Treg cells was significantly lower in patients with T2DM than in healthy controls. The number of T helper cells and lymphocytes decreased in T2DM patients as compared to the healthy controls. Based on the results, the percentage of T cells was higher in T2DM patients than in healthy controls. The expression of CD25 and FOXP3 markers in Treg cells significantly reduced in T2DM patients compared to the healthy controls; however, this decrease was not significant for the CD4 marker. Conversely, the expression of TGF-β cytokine increased in patients with T2DM compared to the healthy controls.
Conclusion The expression of TGF-β and the percentage of CD4 + CD25 + regulatory T cells are impaired in patients with type 2 diabetes.
Highlights
Nazanin Shahnoruzi(google scholar)(pubmed)
Mehdi SalehiNazanin Shahnoruzi(google scholar)(pubmed)
Ali Ganji(google scholar)(pubmed)
Ghasem Mosayebi(google scholar)(pubmed)
Ali Ghazavi(google scholar)(pubmed)
Keywords
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