Higher TIGIT+CD226- γδ T cells in Patients with Acute Myeloid Leukemia
Higher TIGIT+CD226- γδ T cells in Patients with Acute Myeloid Leukemia
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急性髓系白血病患者的 TIGIT( )CD226(-) γ δ T 细胞水平较高
DOI：
10.1080/08820139.2020.1806868
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发表时间：
2020-08-22
影响因子：
2.8
通讯作者：
Li, Yangqiu
中科院分区：
文献类型：
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作者：
Jin, Zhenyi;Lan, Tianbi;Li, Yangqiu
γ δ T细胞的不同结构和功能异质性与其在癌症免疫中的独特作用有关。急性髓系白血病（AML）患者中γ δ T细胞的不同表型尚不清楚。特别是，γ δ T细胞上的共抑制和共刺激受体的表达模式仍然未知。在这项研究中，我们通过免疫检查点共抑制剂TIGIT（T细胞免疫球蛋白和基于免疫受体酪氨酸的抑制性基序结构域）及其竞争性共刺激受体CD 226的表达，分析了不同临床状态的AML患者（包括初治AML，AML未缓解（NR）和AML完全缓解（CR））中γ δ T细胞亚群的分布。我们的数据证明了TIGIT和CD 226在γ δ T细胞上的不平衡分布，在初治AML患者中，CD 226（+）γ δ T细胞减少，TIGIT（+）γ δ T细胞增加，而TIGIT（-）CD 226（+）γ δ T细胞在化疗后达到CR的AML患者中恢复。此外，具有较高TIGIT（+）CD 226（-）γ δ T细胞的患者显示出较低的非M3 AML总生存率，这可能被认为是一种新的预后免疫生物标志物。总之，我们的研究首次揭示了TIGIT/CD 226轴的不平衡可能与AML患者的不同临床结果有关。
The diverse structural and functional heterogeneity of gamma delta T cells is related to their distinct role in cancer immunity. The different phenotypes of gamma delta T cells in patients with acute myeloid leukemia (AML) is far from clear. In particular, the expression pattern of co-inhibitory and co-stimulatory receptors on gamma delta T cells remains unknown. In this study, we analyzed the distribution of gamma delta T cell subsets by expression of the immune checkpoint co-inhibitor TIGIT (T cell immunoglobulin and immunoreceptor tyrosine-based inhibitory motif domain) and its competing co-stimulatory receptor CD226 in AML patients of different clinical statuses (includingde novoAML, AML in non-remission (NR), and AML in complete remission (CR)). Our data demonstrated an imbalanced distribution of TIGIT and CD226 on gamma delta T cells with a decrease in CD226(+)gamma delta T cells and an increase in TIGIT(+)gamma delta T cells inde novoAML patients, while TIGIT(-)CD226(+)gamma delta T cells were restored in AML patients who achieved CR after chemotherapy. Moreover, the patients who had higher TIGIT(+)CD226(-)gamma delta T cells showed lower overall survival rate for non-M3 AML, which may be considered a novel prognostic immune biomarker. In conclusion, our study reveals for the first time that imbalance in the TIGIT/CD226 axis might be related to different clinical outcomes for AML patients.