<?xml version="1.0"?>
<Articles JournalTitle="Acta Medica Iranica">
  <Article>
    <Journal>
      <PublisherName>Tehran University of Medical Sciences</PublisherName>
      <JournalTitle>Acta Medica Iranica</JournalTitle>
      <Issn>0044-6025</Issn>
      <Volume>37</Volume>
      <Issue>2</Issue>
      <PubDate PubStatus="epublish">
        <Year>1999</Year>
        <Month>06</Month>
        <Day>15</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">EVALUATION OF T LYMPHOCYTE SUBSETS IN CHILDREN WITH BETA THALASSEMIA MAJOR</title>
    <FirstPage>73</FirstPage>
    <LastPage>77</LastPage>
    <AuthorList>
      <Author>
        <FirstName></FirstName>
        <LastName>A. Danesh</LastName>
        <affiliation locale="en_US"></affiliation>
      </Author>
      <Author>
        <FirstName></FirstName>
        <LastName>M. Mir-Ahmadian</LastName>
        <affiliation locale="en_US"></affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2015</Year>
        <Month>09</Month>
        <Day>28</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Peripheral blood T lymphocytes and their subsets were studied in 31 patients with beta thalassemia major (age 2-12years) and compared with 14 age-arid sex-matched healthy controls. Three monoclonal antibodies (anti-CD3, anti CD-f, unti-CDS) were simultaneously applied for detection of Th (CD3-, CD4^), Tsk (CD3+, CD8+) and Th/Ts ratio by flow-cytometry respectively. The results of this study showed a slight increase in the number of Tlymphocytes, T 004^, TCDS+, and CD4'*/CDS* ratio; but this increase was not statistically significant (P&gt;0.05). No primary defect in Tcell subsets was detected and it was suggested that continuous regulation of iron balance is an important factor in decreasing immunological disturbance.</abstract>
    <web_url>https://acta.tums.ac.ir/index.php/acta/article/view/1774</web_url>
    <pdf_url>https://acta.tums.ac.ir/index.php/acta/article/download/1774/1767</pdf_url>
  </Article>
</Articles>
