Higher PD-1 expression concurrent with exhausted CD8+ T cells in patients with de novo acute myeloid leukemia

To investigate the association between the T cell inhibitory receptor programmed death 1 (PD-1) and T cell exhaustion status in T cells from patients with acute myeloid leukemia (AML) and AML in complete remission (CR). Surface expression of PD-1 and the exhaustion and immunosenescence markers CD244...

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Veröffentlicht in:Chinese journal of cancer research 2017-10, Vol.29 (5), p.463-470
Hauptverfasser: Tan, Jiaxiong, Chen, Shaohua, Lu, Yuhong, Yao, Danlin, Xu, Ling, Zhang, Yikai, Yang, Lijian, Chen, Jie, Lai, Jing, Yu, Zhi, Zhu, Kanger, Li, Yangqiu
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Sprache:eng
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Zusammenfassung:To investigate the association between the T cell inhibitory receptor programmed death 1 (PD-1) and T cell exhaustion status in T cells from patients with acute myeloid leukemia (AML) and AML in complete remission (CR). Surface expression of PD-1 and the exhaustion and immunosenescence markers CD244 and CD57 on CD3+, CD4+ and CD8+ T cells from peripheral blood samples from 20 newly diagnosed, untreated AML patients and 10 cases with AML in CR was analyzed by flow cytometry. Twenty-three healthy individuals served as control. A significantly higher percentage of PD-1+ cells were found for CD3+ T cells in the AML group compared with healthy controls. In addition, an increased level of PD-1+CD8+ T cells, but not PD-1+CD4+, was found for CD3+ T cells in the AML and AML-CR samples. A higher percentage of CD244+CD4+, CD244+CD8+, CD57+CD4+ and CD57+CD8+ T cells was found in CD3+ T cells in samples from those with AML compared with those from healthy controls. Strong increased PD-1+CD244+ and PD-1+CD57+ co-expression was found for CD4+ and CD8+ T cells in the AML group compared with healthy controls. We characterized the major T cell defects, including co-expression of PD-1 and CD244, CD57-exhausted T cells in patients with AML, and found a particular influence on CD8+ T cells, suggesting a poor anti-leukemia immune response in these patients.
ISSN:1000-9604
1993-0631
DOI:10.21147/j.issn.1000-9604.2017.05.11