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Scrutinizing the Expression and Blockade of Inhibitory Molecules Expressed on T Cells From Acute Myeloid Leukemia Patients Pubmed



Abdolmaleki M1 ; Mojtabavi N2 ; Zavvar M1 ; Vaezi M3 ; Noorbakhsh F1 ; Nicknam MH1, 4
Authors
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Authors Affiliations
  1. 1. Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  2. 2. Department of Immunology, Iran University of Medical Sciences, Tehran, Iran
  3. 3. Hematology, Oncology and Stem Cell Transplantation Research Center, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran
  4. 4. Molecular Immunology Research Center, Tehran University of Medical Sciences, Tehran, Iran

Source: Iranian Journal of Allergy# Asthma and Immunology Published:2018


Abstract

T cell exhaustion is an immunosuppressive mechanism which occurs in chronic viral infections, solid tumors and hematologic malignancies. Exhausted T cell has increased the expression of inhibitory receptors, and functional impairment. In this study, we investigated the expression from some of those inhibitory receptors being Programmed death 1 (PD-1), T cell immunoglobulin and mucin domain containing molecules 3 (TIM-3) and CD244 on T cells from Iranian acute myeloid leukemia (AML) patients. Peripheral blood samples were collected from Iranian newly diagnosed AML patients and flow cytometric analysis was accomplished for cell surface expression of PD-1, TIM-3, and CD244 on T lymphocytes. Functionality and proliferation assay were done in the presence of anti-PD-1 and anti-CD244 blocking antibodies. Immunophenotyping of T cells showed a significant increase of PD-1 and CD244 expression on CD4+ and CD8+ T cells of AML patients. Whereas blockade of PD-1 and CD244 increased the proliferation of CD4+ and CD8+ T lymphocytes of AML patients but IFN-a production was not significantly increased. In conclusion, our data indicate that CD4+ and CD8+ T cells from AML patients appeared to be exhausted and blockade of some immune checkpoints can improve the proliferation of those cells. © June 2018, Iran J Allergy Asthma Immunol. All rights reserved.