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Year : 2017  |  Volume : 30  |  Issue : 3  |  Page : 906-911

Assessment of T-regulatory cells in type 1 diabetes mellitus

1 Department of Clinical Pathology, Faculty of Medicine, Menoufia University, Menoufia, Egypt
2 Department of Pediatrics, Faculty of Medicine, Menoufia University, Menoufia, Egypt

Correspondence Address:
Samar S Salman
Shibin El-Kom, Menoufia, 32511
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1110-2098.218280

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Objective The aim of the study was to evaluate T-regulatory cells (Tregs) expression in the peripheral blood of children with type 1 diabetes mellitus (T1D). Background T1D is mainly a T-cell-mediated autoimmune disease characterized by the destruction of pancreatic β cells leading to insulin deficiency. It is a common autoimmune disorder in childhood, but the disease may become manifest at any age, even in adults. Tregs are subsets of T cells that have an essential role in maintaining tolerance; thus, these cells may play an important role in the pathogenesis of T1D. Patients and methods This study was carried out in the Clinical Pathology Department, Faculty of Medicine, Menoufia University, between August 2014 and November 2015. The study included 50 children, who included 30 children diagnosed as T1D and 20 age-matched and sex-matched apparently healthy children as controls. All children were subjected to complete blood count, glycated hemoglobin evaluation, and surface and cytoplasmic detection of Tregs by flow cytometry. Results This study showed that Tregs (CD4+ CD25+ FoxP3+) decreased in diabetic children in comparison with normal controls (P < 0.001). It also showed a higher decrease in the percentage of Tregs (CD4+ CD25+ FoxP3+) in uncontrolled diabetic children (hemoglobin A1c > 7.0%) in comparison with controlled diabetic children (hemoglobin A1c < 7.0%) (P < 0.001). Conclusion Diminished Tregs proved that breakdown of immune tolerance often leads to the development of autoimmune diseases including T1D, which confirms the essential role of Tregs in the pathogenesis of T1D.

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