Document Type : Original Article
Authors
- Hamideh Mesali 1
- Abolghasem Ajami 1, 2
- Hadi Hussein-Nattaj 1
- Alireza Rafiei 1, 2
- Zeinab Rajabian 1
- Hossein Asgarian-Omran 1
- Vahid Hosseini 3
- Tarang Taghvaei 3
- Mohsen Tehrani 1, 2
1 Department of Immunology, School of Medicine
2 Molecular and Cell Biology Research Center
3 Inflammatory Diseases of Upper Gastrointestinal Tract Research Center, Imam Hospital, Mazandaran University of Medical Sciences, Sari, Iran
Abstract
Background: Regulatory T Cells (Tregs) and Myeloid-Derived Suppressor Cells (MDSCs) are two main regulatory cells modulating the immune responses in inflammation and cancer. Objective: To investigate and compare Tregs and MDSCs in peptic ulcer and gastric cancer.
Methods: Patients with dyspepsia were selected and divided into three groups of non-ulcer dyspepsia (NUD, n=22), peptic ulcer disease (PUD, n=25), and gastric cancer (GC, n=27) according to their endoscopic and histopathological examinations. Helicobacter pylori infection was diagnosed by rapid urease test and histopathology. The number of peripheral blood CD4+CD25+FoxP3+Tregs and CD14+HLA-DR- MDSCs were determined in all patients, by flow cytometry. The number of FoxP3+ regulatory T cells was also determined by immunohistochemistry (IHC).
Results: The percentage of peripheral blood Treg cells in both PUD )0.81 ± 0.39, p<0.001) and GC groups )0.98 ± 0.65, p<0.001) were significantly higher than in NUD group (0.46 ± 0.10). These results were also confirmed by IHC. A significantly higher percentage of MDSCs in patients with PUD )0.73 ± 0.19, p<0.001) and GC )0.73 ± 0.16, p<0.001) was also observed when compared to NUD group )0.46 ± 0.16). There was no difference in the percentages of these two cell types between the PUD and GC groups. The percentages of Tregs and MDSCs in patients with PUD and GC were not significantly correlated. Conclusions: Both Tregs and MDSCs showed higher frequencies in PUD and GC. These results suggest that immune-modulation by the Tregs and MDSCs may play a role in the pathogenesis of PUD and GC.
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