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RESEARCH PAPER
 
 

Impact of treatment with methimazole on the Bcl-2 expression in CD8+ peripheral blood lymphocytes in children with Graves’ disease

Maria Klatka 1,  
 
1
Department of Pediatric Endocrinology and Diabetology,Medical University, Lublin, Poland
2
Department of Clinical Immunology and Immunotherapy, Medical University, Lublin, Poland
Ann Agric Environ Med 2013;20(4):884–888
KEYWORDS:
ABSTRACT:
Introduction and objectives: The protein product of the proto-oncogene Bcl-2 is a physiological inhibitor of programmed cell death. The results obtained in our previous researches suggest that apoptosis may be involved in the regulation of an immune response in hyperthyroidism. The most common cause of hyperthyroidism is Graves’ disease. The aim of this study was evaluation of expression of Bcl-2 protein in peripheral blood T lymphocytes in hyperthyroid children due to Graves’ disease (GD) before and after therapy with methimazole (MMI), in comparison with healthy controls. Material and methods: Thirty-two children with newly diagnosed hyperthyreosis due to GD before and after 4–6 weeks treatment with MMI, and 20 healthy controls were included into the study. The staining with monoclonal antibodies against CD8 and Bcl-2 was performed within 2 hours after collection, and followed with flow cytometry acquisition and analysis. Results: Our study revealed that the expression of Bcl-2 protein in circulating CD8+ T lymphocytes of patients with hyperthyreosis was significantly lower than in healthy controls (p<0.03). The expression of Bcl-2 after 4–6 week therapy with MMI returned to normal level. The difference in Bcl-2 expression between patients after treatment and control group was insignificant. Conclusions: The use of MMI in the treatment of hyperthyroidism due to GD leads to the normalization of the Bcl-2 expression on the CD8+ lymphocytes in peripheral blood. Our findings suggest that the changes in the expression of Bcl-2 on the CD8+ cells indicate the involvement of these cells and Bcl-2-regulated apoptotic pathway in the pathogenesis of GD.
eISSN:1898-2263
ISSN:1232-1966