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" Study of molecular mechanisms of TNF-alpha induced apoptosis in peripheral blood mono nuclear cell from patients with beta thalassemia major "
/مهدی قطره سامانی
; Minoo Adib, Behjat Alsadat Moayedi,, Masood Soleimani
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Isfahan University of Medical Sciences
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| Document Type
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Latin Dissertation
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| Language of Document
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English
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| Record Number
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103514
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| Doc. No
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T15158
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WH,170,G411s,2014
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| Main Entry
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Ghatrehsamani, Mahdi
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| Title & Author
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Study of molecular mechanisms of TNF-alpha induced apoptosis in peripheral blood mono nuclear cell from patients with beta thalassemia major/مهدی قطره سامانی
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| College
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Schools, Medical
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| Date
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, 2014
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| Degree
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Immunology, phD
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60 p.: tab., Diag
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| Note
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This thesis is a research project with project ID: 188143
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| Abstract
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thalassemia major (TM) is a hereditary disease and it characterized by abnormal hemoglobin synthesis, which results in decreased oxygen delivery to the tissues, ineffective erythropoiesis and iron overload. there is increased susceptibility to infections in beta-thalassemia. changes in T and B-lymphocyte subsets and regulatory T cells (treg cells) play a crucial role in the maintenance of immunological self-tolerance. aryl hydrocarbon receptor (AhR)of these cells could be modulated by cytokines. the purpose of this study was to investigate the interaction of tumor necrosis factor alpha (TNF-alpha) with the tetrachlorodibenbzo-p-dioxin (TCDD) and ligand of AhR on peripheral blood lympocytes in patients with beta-thalassemia major. TM patients who were on regular transjusion program were included in the study. flow cytometry was used to determine the apoptosis, necrosis and tumor necrosis factor receptor 1 (TNFR1). the expression of cystein-aspartic proteases-1 (caspase-1), caspase-3, caspase-8, NOD-like receptor family, pyrin domain containing 3 (NLRP3) and AhR were assessed by real time PCR. these results were compared with blood samples from healthy volunteers. our data showed significant differences expression of TNFR1 in beta-thalassemia major compare to control individuals. treatment of control individual lymphocytes with TNF-alpha induced a significant increase in the rate of necrosis mediated by TNFR1 in compare to other groups, whereas co-treatment of TCDD and TNF-alpha significantly decreased necrosis and cell death rather than control groups 1. in contrast co-administered of patient cells with TCDD and TNF-alpha(group 2) significantly increased cell death and necrosis rather than patient group 1. apoptosis was not significant between all groups. collectively our study showed that TCDD significantly inhibit effects of TNF-alpha on apoptosis and AhR expression of lymphocytes. these results showed that chronic inflammation in TM decreased caspase-1 , caspase-3, and caspase-8 expression and also exposure of human lymphocytes to TCDD could help to increase expression of caspase-1, 3.
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| Descriptor
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1. beta-Thalassemia.- Descriptors: beta-Thalassemia
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Receptors, Aryl Hydrocarbon
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Tetrachlorodibenzodioxin
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Tumor Necrosis Factor-alpha
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Lymphocytes
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Apoptosis
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Adib, Minoo, Supervisor
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Moayedi, Behjat Alsadat, Supervisor
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Soleimani, Masood, Supervisor
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| Translated Title Supplied by Cataloguer
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بررسی مکانیسم مولکولی القا آپوپتوز با واسطه TNF-alpha در سلولهای تک هسته ای خون محیطی بیماران مبتلا به تالاسمی ماژور
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