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Altered expression of the TCR signaling related genes CD3 and FcεRIγ in patients with aplastic anemia

DOI: 10.1186/1756-8722-5-6

Keywords: Aplastic anemia, CD3γ, CD3δ, CD3ε, CD3ζ, FcεRIγ, Gene expression

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Abstract:

To elucidate the T cell receptor (TCR) signal transduction features in AA, the expression levels of CD3γ, δ, ε and ζ chain and FcεRIγ genes, which are involved in TCR signal transduction, and the negative correlation of the expression levels between the CD3ζ and FcεRIγ genes in T cells from peripheral blood mononuclear cells (PBMCs) were analyzed. Real-time RT-PCR using the SYBR Green method was used to detect the expression level of these genes in PBMCs from 18 patients with AA and 14 healthy individuals. The β2microglobulin gene (β2M) was used as an endogenous reference. The expression levels of the CD3γ, CD3δ, CD3ε and CD3ζ genes in patients with AA were significantly increased compared to a healthy control group, whereas the FcεRIγ gene expression level was significantly decreased in patients with AA in comparison with the healthy control group. Moreover, the negative correlation of the expression levels between the CD3ζ and FcεRIγ genes was lost.To our knowledge, this is the first report of the CD3γ, CD3δ, CD3ε, CD3ζ and FcεRIγ gene expression in patients with AA. The abnormally expressed TCR signaling related genes may relate to T cells dysfunction in AA.Aplastic anemia (AA) is a potentially fatal bone marrow failure disorder that is characterized by pancytopenia and bone marrow hypoplasia. In most cases, AA behaves as an immune-mediated disease [1]. Immunosuppression is a key treatment strategy for patients who are not suitable bone marrow transplant (BMT) candidates due to age or the lack of a suitable donor. Immunosuppression with antithymocyte globulins and cyclosporine is effective for restoring blood cell production in the majority of patients [2,3]. The thought that T cells play a major role in the pathophysiology of AA became evident in the late 1970s with the finding that marrow and peripheral blood lymphocytes from patients with AA were able to suppress hematopoiesis in vitro. Subsequently, activated CD8+ T cells were identified as the lymphocyte sub

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