Biochemical nature and cellular distribution of the paired immunoglobulin-like receptors, PIR-A and PIR-B.

Biochemical nature and cellular distribution of the paired immunoglobulin-like receptors, PIR-A and PIR-B.
复制标题

配对的免疫球蛋白样受体PIR-A和PIR-B的生化性质和细胞分布。

DOI:
10.1084/jem.189.2.309
复制
发表时间:
1999-01-18
影响因子:
15.3
通讯作者:
Cooper, M D
Cooper, M D
中科院分区:
医学1区
文献类型:
--
作者:
Kubagawa, H;Chen, C C;Ho, L H;Shimada, T S;Gartland, L;Mashburn, C;Uehara, T;Ravetch, J V;Cooper, M D

文献摘要

被引文献

相似文献

PIR-A 和 PIR-B 是配对的免疫球蛋白样受体,分别由小鼠体内的多个 Pira 基因和单个 Pirb ​​基因编码,是人类自然杀伤 (NK) 和 Fc 受体的亲戚。针对重组 PIR 蛋白产生的单克隆和多克隆抗体鉴定出 B 细胞、粒细胞和巨噬细胞上~85 和~120 kD 的细胞表面糖蛋白。与细胞表面 PIR 分子相关的二硫键连接的同二聚体被鉴定为 Fc 受体共同 γ (FcRγc) 链。 PIR-B 成纤维细胞转染子表达约 120 kD 的细胞表面分子,而 PIR-A 转染子仅在细胞内表达约 85 kD 分子; PIR-A 和 FcRγc 共转染子在其细胞表面表达 PIR-A/FcRγc 复合物。相应地,PIR-B 通常在 FcRγc−/− 小鼠脾细胞的细胞表面表达,而 PIR-A 则不然。骨髓细胞和 B 谱系细胞上 PIR 分子的细胞表面水平随着细胞分化和激活而增加。树突状细胞、单核细胞/巨噬细胞和肥大细胞表达不同水平的 PIR 分子,但 T 细胞和 NK 细胞不表达。这些实验定义了 PIR-B(一种抑制性受体)和 PIR-A(一种激活性受体)的协调细胞表达;证明细胞表面 PIR-A 表达需要 FcRγc 链缔合;并表明 FcRγc 链表达水平可能对不同细胞谱系中的 PIR-A/PIR-B 平衡产生不同的影响。
PIR-A and PIR-B, paired immunoglobulin-like receptors encoded, respectively, by multiple Pira genes and a single Pirb gene in mice, are relatives of the human natural killer (NK) and Fc receptors. Monoclonal and polyclonal antibodies produced against a recombinant PIR protein identified cell surface glycoproteins of ∼85 and ∼120 kD on B cells, granulocytes, and macrophages. A disulfide-linked homodimer associated with the cell surface PIR molecules was identified as the Fc receptor common γ (FcRγc) chain. Whereas PIR-B fibroblast transfectants expressed cell surface molecules of ∼120 kD, PIR-A transfectants expressed the ∼85-kD molecules exclusively intracellularly; PIR-A and FcRγc cotransfectants expressed the PIR-A/ FcRγc complex on their cell surface. Correspondingly, PIR-B was normally expressed on the cell surface of splenocytes from FcRγc−/− mice whereas PIR-A was not. Cell surface levels of PIR molecules on myeloid and B lineage cells increased with cellular differentiation and activation. Dendritic cells, monocytes/macrophages, and mast cells expressed the PIR molecules in varying levels, but T cells and NK cells did not. These experiments define the coordinate cellular expression of PIR-B, an inhibitory receptor, and PIR-A, an activating receptor; demonstrate the requirement of FcRγc chain association for cell surface PIR-A expression; and suggest that the level of FcRγc chain expression could differentially affect the PIR-A/PIR-B equilibrium in different cell lineages.