Human leukocyte antigen-B-associated transcript 3 is released from tumor cells and engages the NKp30 receptor on natural killer cells
Human leukocyte antigen-B-associated transcript 3 is released from tumor cells and engages the NKp30 receptor on natural killer cells
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DOI：
10.1016/j.immuni.2007.10.010
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发表时间：
2007-12-01
期刊：
影响因子：
32.4
通讯作者：
Engert, Andreas
中科院分区：
文献类型：
--
作者：
von Strandmann, Elke Pogge;Simhadri, Venkateswara Rao;Engert, Andreas
自然杀伤（NK）细胞的活性受表面受体调节，其指导靶细胞识别。NKp 30（天然细胞毒性受体3）诱导靶细胞溶解，也是与树突状细胞相互作用的关键。到目前为止，NKp 30的细胞配体仍然难以捉摸。在这里，我们表明，核因子HILA-B相关的转录本3（BAT 3）从肿瘤细胞释放，直接结合到NKp 30，并参与NK细胞上的NKp 30。BAT 3触发NKp 30介导的细胞毒性，并且是多发性骨髓瘤模型中肿瘤排斥所必需的。这些数据将BAT 3鉴定为NKp 30的细胞配体。我们提出了一个概念，通过NK细胞识别靶细胞超越“丢失自我”和“诱导自我”，通过肿瘤细胞衍生的细胞外因子介导。
The activity of natural killer (NK) cells is regulated by surface receptors, which direct target cell recognition. NKp30 (Natural Cytotoxicity Receptor 3) induces target cell lysis and is also crucial for the interaction with dendritic cells. So far, the cellular ligands for NKp30 have remained elusive. Here we show that the nuclear factor HILA-B-associated transcript 3 (BAT3) was released from tumor cells, bound directly to NKp30, and engaged NKp30 on NK cells. BAT3 triggered NKp30-mediated cytotoxicity and was necessary for tumor rejection in a multiple myeloma model. These data identify BAT3 as a cellular ligand for NKp30. We propose a concept for target cell recognition by NK cells beyond "missing self" and "induced self," mediated through a tumor cell-derived extracellular factor.