Human leukocyte antigen-B-associated transcript 3 is released from tumor cells and engages the NKp30 receptor on natural killer cells

被引：262

作者：

von Strandmann, Elke Pogge ^{[1
]}

Simhadri, Venkateswara Rao ^{[1
]}

von Tresckow, Bastian ^{[1
]}

Sasse, Stephanie ^{[1
]}

Reiners, Katrin S. ^{[1
]}

Hansen, Hinrich P. ^{[1
]}

Rothe, Achim ^{[1
]}

Boell, Boris ^{[1
]}

Simhadri, Vijaya Lakshmi ^{[1
]}

Borchmann, Peter ^{[1
]}

McKinnon, Peter J. ^{[2
]}

Hallek, Michael ^{[1
]}

Engert, Andreas ^{[1
]}

机构：

[1] Univ Hosp Cologne, Dept Internal Med 1, D-50924 Cologne, Germany

[2] St Jude Childrens Res Hosp, Dept Genet & Tumor Cell Biol, Memphis, TN 38105 USA

来源：

IMMUNITY | 2007年 / 27卷 / 06期

关键词：

D O I：

10.1016/j.immuni.2007.10.010

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

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.

引用

页码：965 / 974

页数：10

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