Phenotypic Analysis of Lymphocyte Populations in Type 1 Diabetes Mellitus
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Abstract
Type 1 Diabetes Mellitus (T1D) is a T cell-mediated autoimmune disease and is one of the most frequent chronic diseases of children and young adults. It results from immune-mediated destruction of the insulin-producing pancreatic beta cells. Aim of the work: This study aims to establish the phenotypic characteristics of various lymphocyte populations in type1 Diabetes Mellitus and try to correlate between the lymphocyte populations, patients’ age and duration of the disease. Patients and Methods: The study included 30 children with type 1 Diabetes and 20 healthy control children who were tested for peripheral blood lymphocytes using flow- cytometry. The percentages of total T-lymphocytes, B-lymphocytes, helper T cells, cytotoxic T cells, activated T lymphocytes, regulatory T cells and natural killer cells were evaluated with the use of CD3, CD19, CD4, CD8, CD25, CD127, HLA-DR and CD56 monoclonal antibodies, respectively. Results: No significant difference was found in the percentage of different lymphocyte subpopulations in diabetic patients and controls except for T-regulatory cells that decreased significantly in patients (2.28 ± 0.37) when compared to healthy controls (3.12 ± 0.34), with a p value of 0.045 and activated cytotoxic T cells that increased significantly in diabetic patients (11.17 ± 0.73) in comparison to healthy controls (8.67 ± 1.06) with a p value of 0.02. In addition, no correlations of lymphocyte populations with patients’ age and duration of the disease were found except for natural killer cells that showed significant negative correlation.
Conclusion: The differences detected in some lymphocyte subpopulations support the role of cellular autoimmune mechanisms in the pathogenesis of the disease.
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How to Cite This Article
Ahmed Hassan, Mohamed Abdelal, Tamer Mohamed, Heba Assaghir, Hydi Ahmed (2014); Phenotypic Analysis of Lymphocyte Populations in Type 1 Diabetes Mellitus, Int. J. of Adv. Res., 2 (05), 0, ISSN 2320-5407.
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This work is licensed under a Creative Commons Attribution 4.0 International License.





