Shiratori Ikuo, Ogasawara Kouetsu, Saito Takashi, Lanier Lewis L, Arase Hisashi
Department of Molecular Genetics, Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuoku, 260-8670, Japan.
J Exp Med. 2004 Feb 16;199(4):525-33. doi: 10.1084/jem.20031885.
Paired receptors that consist of highly related activating and inhibitory receptors are widely involved in the regulation of the immune system. Here, we report a mouse orthologue of the human activating paired immunoglobulin-like type 2 receptor (PILR) beta, which was cloned from a cDNA library of natural killer (NK) cells based on its ability to associate with the DAP12 signaling adaptor protein. The activating PILRbeta was expressed not only on NK cells but also on dendritic cells and macrophages. Furthermore, we have identified a novel CD99-like molecule as a ligand for the activating PILRbeta and inhibitory PILRalpha receptors. Transcripts of PILR ligand are present in many tissues, including some T cell lines. Cells expressing the PILR ligand specifically activated NK cells and dendritic cells that express the activating PILRbeta. Our findings reveal a new regulatory mechanism of innate immunity by PILR and its CD99-like ligand.
由高度相关的激活受体和抑制受体组成的配对受体广泛参与免疫系统的调节。在此，我们报道了人类激活型配对免疫球蛋白样2型受体（PILR）β的小鼠同源物，它是基于其与DAP12信号衔接蛋白结合的能力，从自然杀伤（NK）细胞的cDNA文库中克隆得到的。激活型PILRβ不仅在NK细胞上表达，还在树突状细胞和巨噬细胞上表达。此外，我们鉴定出一种新型的CD99样分子作为激活型PILRβ和抑制型PILRα受体的配体。PILR配体的转录本存在于许多组织中，包括一些T细胞系。表达PILR配体的细胞特异性激活表达激活型PILRβ的NK细胞和树突状细胞。我们的发现揭示了PILR及其CD99样配体对固有免疫的一种新的调节机制。
