Masuda Ai, Nakamura Akira, Maeda Tsutomu, Sakamoto Yuzuru, Takai Toshiyuki
Department of Experimental Immunology, Japan Science and Technology Agency, Tohoku University, Aoba-ku, Sendai-shi 980-8575, Japan.
J Exp Med. 2007 Apr 16;204(4):907-20. doi: 10.1084/jem.20060631. Epub 2007 Apr 9.
Allergy is caused by immune effector cells, including mast cells and basophils. Cellular signaling that activates these effector cells is regulated by different inhibitory receptors on their surface. We show that human leukocyte immunoglobulin (Ig)-like receptor (LILR) B2 and its mouse orthologue, paired Ig-like receptor (PIR)-B, constitutively associate to major histocompatibility complex (MHC) class I on the same cell surface (in cis). The IgE-mediated effector responses were augmented in beta(2)-microglobulin (beta(2)m) and PIR-B-deficient mast cells. In addition, the increased cytokine production of beta(2)m-deficient mast cells was not affected by the co-culture with MHC class I-positive mast cells, showing that less cis interaction between PIR-B and MHC class I on mast cells led to the increased cytokine release. Thus, the constitutive cis binding between LILRB2 or PIR-B and MHC class I has an essential role in regulating allergic responses.
过敏是由免疫效应细胞引起的，包括肥大细胞和嗜碱性粒细胞。激活这些效应细胞的细胞信号传导受其表面不同抑制性受体的调节。我们发现人类白细胞免疫球蛋白（Ig）样受体（LILR）B2及其小鼠同源物配对Ig样受体（PIR）-B在同一细胞表面（顺式）与主要组织相容性复合体（MHC）I类组成性结合。在β2微球蛋白（β2m）和PIR-B缺陷的肥大细胞中，IgE介导的效应反应增强。此外，β2m缺陷的肥大细胞中细胞因子产生的增加不受与MHC I类阳性肥大细胞共培养的影响，这表明肥大细胞上PIR-B与MHC I类之间较少的顺式相互作用导致细胞因子释放增加。因此，LILRB2或PIR-B与MHC I类之间的组成性顺式结合在调节过敏反应中起重要作用。
