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Iranian Journal of Allergy, Asthma and Immunology، جلد ۱۳، شماره ۲، صفحات ۸۵-۹۲
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عنوان انگلیسی Alteration in frequency and function of CD4⁺CD25⁺FOXP3⁺ regulatory T cells in patients with immune thrombocytopenic purpura.
چکیده انگلیسی مقاله Immune thrombocytopenic  purpura (ITP) is an autoimmune bleeding disorder characterized by production  of auto-antibodies against platelet antigens. It is obvious that regulatory T cells (Tregs) have a major role in controlling immune homeostasis and preventing autoimmunity. To investigate the frequency and functions of Tregs, twenty ITP patients and twenty age- and sex- matched healthy controls were recruited. The peripheral blood mononuclear cells were isolated and the proportion of Tregs was defined by flow cytometry method. The expression of immune-regulatory markers, cytotoxic T-lymphocyte associated antigen-4 (CTLA-4) and glucocorticoid induced tumor necrosis  factor  receptor  (GITR)  were  also  assessed by  quantitative  Real-time polymerase chain reaction TaqMan method. For evaluation of Treg function, Tregs were enriched and their ability to inhibit proliferation of T cells was measured and levels of immune-regulatory cytokines IL-10 and Transforming growth factor beta (TGF-β) were also measured.Results showed that the frequency of Tregs  and  the  mean  fluorescence  intensity  of  forkhead  box  P3  (FOXP3)  protein  significantly decreased in ITP patients compared to those in healthy controls. In addition, there was a significant reduction  in relative expression of both  CTLA-4 and GITR  mRNA  in ITP  patients (p=0.02 and p=0.006, respectively). The suppressive function of Tregs also diminished in ITP patients compared to controls. Both  IL-10 and TGF-β  cytokines were produced  in lower amounts  in ITP  patients than controls. It  could  be  concluded  that  alteration  in  Treg  frequency and  functional  characteristics might  be responsible for loss of self-tolerance and subsequently destructive immune responses observed in ITP patients.
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نویسندگان مقاله | Nargess Arandi
Department of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran


| Abbas Mirshafiey
Department of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran


| Mahmood Jeddi-Tehrani
Monoclonal Antibody Research Center, Avicenna Research Institute, ACECR, Tehran, Iran


| Mohammadreza Shaghaghi
Research Center for Immunodeficiency, Pediatrics Center of Excellence, Children’s Medical Center, Tehran University of Medical Sciences, Tehran, Iran


| Bamdad Sadeghi
Research Center for Immunodeficiency, Pediatrics Center of Excellence, Children’s Medical Center, Tehran University of Medical Sciences, Tehran, Iran


| Hassan Abolhassani
Research Center for Immunodeficiency, Pediatrics Center of Excellence, Children’s Medical Center, Tehran University of Medical Sciences, Tehran, Iran


| Ramazan Ali Sharifian
Clinic of Hematology and Oncology, Vali-Asr Hospital, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran


| Mohammad Saeid Rahiminejad
Division of Pediatric Hematology Oncology, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran


| Asghar Aghamohammadi
Research Center for Immunodeficiency, Pediatrics Center of Excellence, Children’s Medical Center, Tehran University of Medical Sciences, Tehran, Iran
نشانی اینترنتی http://ijaai.tums.ac.ir/index.php/ijaai/article/view/472
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