HLA-C与CD160受体的结合是循环自然杀伤（NK）细胞用于介导细胞毒性的触发机制。
Engagement of CD160 receptor by HLA-C is a triggering mechanism used by circulating natural killer (NK) cells to mediate cytotoxicity.
作者信息
Le Bouteiller Philippe, Barakonyi Aliz, Giustiniani Jérome, Lenfant Françoise, Marie-Cardine Anne, Aguerre-Girr Maryse, Rabot Magali, Hilgert Ivan, Mami-Chouaib Fathia, Tabiasco Julie, Boumsell Laurence, Bensussan Armand
机构信息
Institut National de la Santé et de la Recherche Médicale U563, Hôpital Purpan, 31059 Toulouse Cedex 3, France.
出版信息
Proc Natl Acad Sci U S A. 2002 Dec 24;99(26):16963-8. doi: 10.1073/pnas.012681099. Epub 2002 Dec 16.
Circulating human natural killer (NK) lymphocytes have been functionally defined by their ability to exert cytotoxic activity against MHC class I-negative target cell lines, including K562. Therefore, it was proposed that NK cells recognized the "missing self." We show here that the Ig-like CD160 receptor expressed by circulating CD56(dim+) NK cells or IL-2-deprived NK cell lines is mainly involved in their cytotoxic activity against K562 target cells. Further, we report that HLA-C molecules that are constitutively expressed by K562 trigger NK cell lysis through CD160 receptor engagement. In addition, we demonstrate, with recombinant soluble HLA-Cw3 and CD160 proteins, direct interaction of these molecules. We also find that CD158b inhibitory receptors partially interfere with CD160-mediated cytotoxicity, whereas CD94CD159a and CD85j have no effect on engagement with their respective ligands. Thus, CD160HLA-C interaction constitutes a unique pathway to trigger NK cell cytotoxic activity.
循环中的人类自然杀伤（NK）淋巴细胞的功能定义为其对包括K562在内的MHC I类阴性靶细胞系发挥细胞毒性活性的能力。因此，有人提出NK细胞识别“缺失的自我”。我们在此表明，循环中的CD56（dim +）NK细胞或白细胞介素-2剥夺的NK细胞系所表达的免疫球蛋白样CD160受体主要参与其对K562靶细胞的细胞毒性活性。此外，我们报告说，K562组成性表达的HLA - C分子通过CD160受体结合触发NK细胞裂解。另外，我们用重组可溶性HLA - Cw3和CD160蛋白证明了这些分子的直接相互作用。我们还发现，CD158b抑制性受体部分干扰CD160介导的细胞毒性，而CD94CD159a和CD85j对与其各自配体的结合没有影响。因此，CD160 - HLA - C相互作用构成了触发NK细胞细胞毒性活性的独特途径。
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