期刊
JOURNAL OF IMMUNOLOGY
卷 182, 期 11, 页码 6727-6735出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.0900212
关键词
-
类别
资金
- Etablissement Francais du Sang
- Universite de Nantes
- Ligue contre le Cancer
- Nantes Atlantique Greffe de Moelle Osseuse association
- Comite Departemental de Loire-Atlantique de la Ligue contre le Cancer
Recently, the Z27 mAb was shown to recognize the NK cell-activating receptor KIR3DS1, and several genetic studies suggest that the most probable ligands of KIR3DS1 are HLA class I molecules with the Bw4 motif. Despite these findings, the attempts to establish a functional interaction between KIR3DS1 and its potential ligand have been unsuccessful. Here, we study the proliferation and cytotoxicity of KIR3DS1(+) NK cells, compared with KIR3DL1(+) NK cells, according to the Bw4(+) or Bw4(-) allogeneic environment. Our results show for the first time that KIR3DS1 expression on NK cells can be induced after exposure to stimulator cells (221, K562, EBV-B cell lines, and B cells), polyinosinic-polycytidylic acid, IL-15, or IL-2. Furthermore, whereas KIR3DL1(+) NK cell proliferation and cytotoxicity were inhibited in a Bw4(+) but not a Bw4(-) context, KIR3DS1+ NK cell functions were not influenced by the presence of Bw4 on target cells. Nevertheless, despite the absence of demonstrated regulation of KIR3DS1(+) NK cell functions by HLA-Bw4 molecules, we found a higher KIR3DS1(+) NK cell frequency and higher levels of KIR3DS1 expression in Bw4(+) compared with Bw4(-) individuals. Altogether, these results suggest that K1R3DS1 does not recognize HLA-Bw4 molecules in a physiological context, and they highlight the induced expression of K1R3DS1 observed on stimulated NK cells and the higher frequency of KIR3DS1(+) NK cells in Bw4(+) individuals. Because a protective KIR3DS1-Bw4 association has been reported in viral infections, our results further the understanding of the role of KIR3DS1(+) NK cells in controlling viral infections. The Journal of Immunology, 2009, 182: 6727-6735.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据