ArticleDNA and cell biology2012
Upregulated TCRζ enhances interleukin-2 production in T-cells from patients with CML.
Article in DNA and cell biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Alteration of gene expression profile in CD3ImmunoTargets and therapy · 2018Article
- Enhancement of the TCRζ expression, polyclonal expansion, and activation of t cells from patients with acute myeloid leukemia after IL-2, IL-7, and IL-12 induction.DNA and cell biology · 2015Article
- Upregulated TCRζ improves cytokine secretion in T cells from patients with AML.Journal of hematology & oncology · 2015Article
- Alteration of gene expression profile following PPP2R5C knockdown may be associated with proliferation suppression and increased apoptosis of K562 cells.Journal of hematology & oncology · 2015Article
- Characteristics of TCRζ, ZAP-70, and FcɛRIγ gene expression in patients with T- and NK/T-cell lymphoma.DNA and cell biology · 2015Article
- SEA antagonizes the imatinib-meditated inhibitory effects on T cell activation via the TCR signaling pathway.BioMed research international · 2014Article
- Differential gene expression profiles of PPP2R5C-siRNA-treated malignant T cells.DNA and cell biology · 2013Article
- Proliferation inhibition and apoptosis induction of imatinib-resistant chronic myeloid leukemia cells via PPP2R5C down-regulation.Journal of hematology & oncology · 2013Article
- Changes in the MALT1-A20-NF-κB expression pattern may be related to T cell dysfunction in AML.Cancer cell international · 2013Article
- New insights into antigen specific immunotherapy for chronic myeloid leukemia.Cancer cell international · 2012Article
- Alternative expression of TCRζ related genes in patients with chronic myeloid leukemia.Journal of hematology & oncology · 2012Article
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8 authors.
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Abstract
T-cell immunodeficiency is a common feature in patients with chronic myeloid leukemia (CML), and deficiency in CD3 levels was detected in T cells from these patients, which may represent a characteristic that is related to a lower T cell activation. In this study, we explored the possibility that forced TCRζ gene expression may upreg-u-late T cell receptor (TCR) signaling activation and reverse interleukin-2 (IL-2) production in T cells from patients with CML. A recombinant eukaryotic vector expressing TCRζ was transfected into T cells by nucleofection. Phosphorylated TCRζ, phosphorylated NF-κB, and the IL-2 level in TCRζ-transfected CD3+T cells that were activated with anti-CD3 and anti-CD28 antibodies were measured by Western blot and enzyme-linked immunosorbent assay (ELISA). Significantly increased TCRζ levels were found in TCRζ-transfected CD3+T cells. After CD3 and CD28 antibody stimulation, a significantly higher phosphorylated TCRζ chain level was demonstrated, and an increased IL-2 production in TCRζ-upregulated T cells was associated with the increased expression of the phosphorylated NF-κB. In conclusion, TCRζ gene transfection could restore TCRζ chain deficiency and enhance IL-2 production in T cells from patients with CML. It is possible that TCRζ chain reconstitution in leukemia-specific, clonally expanded T cells will effectively increase their activation of antileukemia cytotoxicity.
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