A novel functional cell surface dimer (Kp43) expressed by natural killer cells and T cell receptor-gamma/delta+ T lymphocytes. I. Inhibition of the IL-2-dependent proliferation by anti-Kp43 monoclonal antibody.
A novel functional cell surface dimer (Kp43) expressed by natural killer cells and T cell receptor-gamma/delta+ T lymphocytes. I. Inhibition of the IL-2-dependent proliferation by anti-Kp43 monoclonal antibody.
复制标题
由自然杀伤细胞和 T 细胞受体 - γ/δ T 淋巴细胞表达的新型功能性细胞表面二聚体 (Kp43)。
作者：
J. Aramburu;M. Balboa;A. Ramirez;Augusto Silva;A. Acevedo;F. Sánchez‐Madrid;M. Landázuri;M. López
在本研究中，我们描述了一种新的功能性细胞表面分子，命名为Kp 43，它是由NK细胞，TCR-γ/δ + T淋巴细胞，和一些CD 8 + CD 56 + TCR-α/β + T细胞克隆的白细胞中表达。Kp 43 Ag是一种70 kDa二硫键连接的二聚体，在还原条件下在SDS-PAGE中迁移为单一的43 kDa条带。新鲜PBL的双色免疫荧光染色显示，只有一部分CD 16+和TCR-γ/δ + T淋巴细胞表达Ag。TCR-α/β + T细胞克隆的分析显示，小部分（20个中的2个）弱表达Kp 43以及CD 8和CD 56分子。通过免疫过氧化物酶染色的不同组织的抗Kp 43，反应性检测仅在淋巴器官，少数分散的细胞被染色，并在一些肝窦细胞。当用B类淋巴母细胞系刺激时，基本上所有NK细胞都获得Kp 43。相比之下，Kp 43的分布模式在T-γ/δ淋巴细胞的体外培养后保持稳定，因此根据其表达描绘了两个子集。在淋巴因子激活的杀伤细胞群体中，通过用高浓度IL-2培养PBL或NK细胞获得，大多数CD 16+和CD 56+细胞变为Kp 43+。Kp 43特异性mAb抑制培养的NK和TCR-γ/δ + T细胞的IL-2依赖性增殖反应，而不影响其非MHC限制性细胞毒性。胃蛋白酶消化的F（ab '）2片段也介导的部分抑制作用在还原为Fab时丧失。抗Kp 43 mAb不干扰IL-2与其表面受体的特异性结合。总之，数据指出Kp 43二聚体参与NK细胞和TCR-γ/δ + T淋巴细胞亚群的IL-2依赖性增殖应答的调节。
In the present study we describe a novel functional cell surface molecule, designated as Kp43, which is expressed among leukocytes by NK cells, TCR-gamma/delta + T lymphocytes, and some CD8+ CD56+TCR-alpha/beta + T cell clones. The Kp43 Ag is a 70-kDa disulfide-linked dimer, which migrates in SDS-PAGE under reducing conditions as a single 43-kDa band. Two-color immunofluorescence staining of fresh PBL revealed that only a fraction of CD16+, and of TCR-gamma/delta + T lymphocytes expressed the Ag. The analysis of TCR-alpha/beta + T cell clones showed that a small proportion (2 out of 20) weakly expressed Kp43 together with the CD8 and CD56 molecules. By immunoperoxidase staining of different tissues the anti-Kp43, reactivity was detected exclusively in lymphoid organs, where a minority of scattered cells was stained, and in some liver sinusoidal cells. Essentially all NK cells acquired Kp43 when stimulated with a B lymphoblastoid cell line. By contrast, the pattern of distribution of Kp43 remained stable upon in vitro culture of T-gamma/delta lymphocytes, thus delineating two subsets according to its expression. In lymphokine-activated killer populations, obtained by culturing either PBL or NK cells with high concentration of IL-2, most CD16+ and CD56+ cells became Kp43+. The Kp43-specific mAb inhibited the IL-2-dependent proliferative response of cultured NK and TCR-gamma/delta + T cells without affecting their non-MHC-restricted cytotoxicity. The partial inhibitory effect, which was mediated as well by pepsin digested F(ab')2 fragments, was lost upon reduction to Fab. The anti-Kp43 mAb did not interfere with the specific binding of IL-2 to its surface receptors. Altogether the data point out that the Kp43 dimer is involved in the regulation of the IL-2-dependent proliferative response of NK cells and a subset of TCR-gamma/delta + T lymphocytes.