Spontaneous loss and alteration of antigen receptor expression in mature CD4+ T cells.

DOI PDF 被引用文献6件
  • S Kyoizumi
    Department of Radiobiology, Radiation Effects Research Foundation, Hiroshima, Japan.
  • M Akiyama
    Department of Radiobiology, Radiation Effects Research Foundation, Hiroshima, Japan.
  • Y Hirai
    Department of Radiobiology, Radiation Effects Research Foundation, Hiroshima, Japan.
  • Y Kusunoki
    Department of Radiobiology, Radiation Effects Research Foundation, Hiroshima, Japan.
  • K Tanabe
    Department of Radiobiology, Radiation Effects Research Foundation, Hiroshima, Japan.
  • S Umeki
    Department of Radiobiology, Radiation Effects Research Foundation, Hiroshima, Japan.

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<jats:p>The TCR/CD3 complex plays a central role in antigen recognition and activation of mature T cells, and, therefore, abnormalities in the expression of the complex should induce unresponsiveness of T cells to antigen stimulus. Using flow cytometry, we detected and enumerated variant cells with loss or alteration of the surface TCR/CD3 expression among human mature CD4+ T cells. The presence of variant CD4+ T cells was demonstrated by isolating and cloning them from peripheral blood, and their abnormalities can be accounted for by alterations in TCR expression such as defects of protein expression and partial protein deletion. The variant frequency in peripheral blood increased with aging in normal donors and was highly elevated in patients with ataxia telangiectasia, an autosomal recessive inherited disease with defective DNA repair and variable T cell immunodeficiency. These findings suggest that such alterations in TCR expression are induced by somatic mutagenesis of TCR genes and can be important factors related to age-dependent and genetic disease-associated T cell dysfunction.</jats:p>

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