Expression Feature of CD3 and FcεRIγ Genes in Patients with Aplastics Anemia

Abstract 4372

Aplastic anemia (AA) is characterized by pancytopenia and bone marrow hypoplasia, resulting from immune-mediated suppression of hematopoiesis. Understanding of the immune pathophysiology, especially T-cell immune of the disease over the past 3 decades have led to improvement the treatment of AA. However, primary and secondary failures after immunosuppressive therapy remain frequent. Thereby, more knowledge of the immune mechanisms leading to the aplastic anemia is crucial to more understanding the mechanism of the disease. In order to elucidate the feature of TCR signal transduction in AA, the expression levels of CD3γ, δ, ε and ζ chain and FcεRIγ genes which involed in TCR signal transduction and negative correlation of the expression levels between CD3ζ and FcεRIγ genes in actived T-cell in peripheral blood mononuclear cells (PBMCs) were analyzed. Real-time RT-PCR with SYBR Green technique was used for detecting the gene expression level in PBMCs from 27 patients with AA and 9 healthy individuals. The β2-microglobulin gene (β2M) was used as an endogenous reference. The expression levels of CD3γ, CD3ε and CD3ζ gene in AA patients (19.96±21.46, 17.50±17.53 and 5.50±3.53, respectively) were significant increased compared with healthy group (4.00±1.70, 4.48±2.37 and 1.95±1.77, respectively) (P< 0.01), whereas the expression level of FcεRIγ gene was significant decreased in AA patients (17.58±10.23) in comparison with healthy group (40.20±25.46) (P< 0.01), while no significant difference of the CD3δ expression level was detected between AA and healthy groups. Moreover, there was lost the negative correlation of the expression levels between CD3ζ and FcεRIγ genes (r=0.19,p=0.33). In conclusions, this is, to our knowledge, the first description of the feature of CD3γ, CD3δ, CD3ε, CD3ζ and FcεRIγ gene expression in AA patients. The abnormality expression of CD3γ, CD3ε, CD3ζand FcεRIγ gene might related to the T-cell dysfunction in AA. Further research is needed to investigate the different expression pattern of these genes in different subset of T cells.