KIR3DL2/CpG ODN Interaction Mediates Sezary Syndrome Malignant T Cell Apoptosis
KIR3DL2/CpG ODN Interaction Mediates Sezary Syndrome Malignant T Cell Apoptosis
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DOI：
10.1038/jid.2014.286
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发表时间：
2015-01-01
影响因子：
6.5
通讯作者：
Marie-Cardine, Anne
中科院分区：
文献类型：
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作者：
Ghazi, Bouchra;Thonnart, Nicolas;Marie-Cardine, Anne
我们以前确定NK细胞受体KIR3DL2作为一个有价值的诊断和预后标志物，用于检测Sezary综合征（SS）患者的肿瘤T细胞负荷。然而，该受体对恶性T淋巴细胞群体的功能仍有待研究。我们在这里证明，其最近确定的配体CpG寡脱氧核苷酸（ODN）的KIR3DL2的参与诱导受体的内化，并导致恶性T细胞的半胱天冬酶依赖性凋亡。这种细胞死亡的过程与转录因子STAT3（信号转导子和转录激活子3）的去磷酸化相关，其在Sezary细胞中被发现组成性磷酸化和激活。我们的研究结果表明，KIR3DL2可以通过使用CpG ODN直接促进SS恶性细胞死亡。
We previously identified the NK cell receptor KIR3DL2 as a valuable diagnostic and prognostic marker for the detection of the tumoral T cell burden of Sezary syndrome (SS) patients. However, the function of this receptor on the malignant T lymphocyte population remained unexplored. We here demonstrate that engagement of KIR3DL2 by its recently identified ligand CpG oligodeoxynucleotide (ODN) induces the internalization of the receptor and leads to a caspase-dependent apoptosis of malignant T cells. This process of cellular death is correlated to a dephosphorylation of the transcription factor STAT3 (signal transducer and activator of transcription 3), which is found constitutively phosphorylated and activated in Sezary cells. Our results indicate that KIR3DL2 can directly promote SS malignant cell death through the use of CpG ODN.