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KIR3DL2/CpG ODN 相互作用介导 Sézary 综合征恶性 T 细胞凋亡。

KIR3DL2/CpG ODN interaction mediates Sézary syndrome malignant T cell apoptosis.

机构信息

INSERM U976, Saint Louis Hospital, Paris, France.

INSERM U976, Saint Louis Hospital, Paris, France; University Paris Diderot, Sorbonne Paris Cité, Paris, France.

出版信息

J Invest Dermatol. 2015 Jan;135(1):229-237. doi: 10.1038/jid.2014.286. Epub 2014 Jul 9.

Abstract

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 Sézary 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 Sézary cells. Our results indicate that KIR3DL2 can directly promote SS malignant cell death through the use of CpG ODN.

摘要

我们之前已经确定了 NK 细胞受体 KIR3DL2 是检测蕈样肉芽肿(SS)患者肿瘤 T 细胞负担的有价值的诊断和预后标志物。然而,这个受体在恶性 T 淋巴细胞群上的功能仍未被探索。我们在这里证明,其最近确定的配体 CpG 寡脱氧核苷酸(ODN)与 KIR3DL2 的结合诱导受体内化,并导致恶性 T 细胞的 caspase 依赖性凋亡。这种细胞死亡过程与转录因子 STAT3(信号转导和转录激活因子 3)的去磷酸化相关,该因子在 SS 细胞中持续磷酸化和激活。我们的结果表明,KIR3DL2 可以通过 CpG ODN 直接促进 SS 恶性细胞死亡。

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