Four epitopes on the rat 55‐kDa subunit of the interleukin 2 receptor as defined by newly developed mouse anti‐rat interleukin 2 receptor monoclonal antibodies

Four epitopes on the rat 55‐kDa subunit of the interleukin 2 receptor as defined by newly developed mouse anti‐rat interleukin 2 receptor monoclonal antibodies
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由新开发的小鼠抗大鼠白细胞介素 2 受体单克隆抗体定义的白细胞介素 2 受体的大鼠 55-kDa 亚基上的四个表位

DOI:
10.1002/eji.1830171123
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发表时间:
1987
影响因子:
5.4
通讯作者:
T. Diamantstein
T. Diamantstein
中科院分区:
医学3区
文献类型:
--
作者:
A. Mouzaki;T. Diamantstein

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针对大鼠白细胞介素2受体(IL 2 R)的四种新的小鼠单克隆抗体(mAb)ART-38、ART-35、ART-75和ART-94已被开发。如免疫沉淀研究所示,它们都特异性识别大鼠IL 2 R的55 kDa亚基。将这些mAb与三种先前表征的针对大鼠IL 2 R的55-kDa分子的小鼠mAb(即ART-18、ART-65和OX-39 mAb)进行比较。在所有7种mAb中,发现仅ART-18和OX-39抑制IL 2与活化的T细胞的结合,而IL 2 R单独抑制ART-18的结合。ART-18是发现的唯一抑制携带IL 2 R的细胞的IL 2依赖性增殖的mAb。Scatchard图分析显示mAb结合位点数量的总体差异范围为30000(ART-65)至165000(ART-75),其亲和力范围为2.5 × 10−9 M(ART-38)至8.3 × 10−10 M(OX-39)。交叉抑制研究显示,mAb识别55-kDa大鼠IL 2 R亚基上的四种不同表位。
Four new mouse monoclonal antibodies (mAb), ART‐38, ART‐35, ART‐75 and ART‐94, directed against the rat interleukin 2 receptor (IL 2R) have been developed. As shown by immunoprecipitation studies they all recognize specifically the 55‐kDa subunit of the rat IL 2R. These mAb were compared to three previously characterized mouse mAb directed against the 55‐kDa molecule of the rat IL 2R, namely the ART‐18, ART‐65 and OX‐39 mAb. Out of all seven mAb, only ART‐18 and OX‐39 were found to inhibit the IL 2 binding to activated T cells, while IL 2R inhibited the binding of ART‐18 alone. ART‐18 was the only mAb found to inhibit the IL 2‐dependent proliferation of cells carrying the IL 2R. Scatchard plot analyses showed gross differences in the numbers of mAb‐binding sites ranging between 30000 (ART‐65) and 165000 (ART‐75) as well as in their affinities which ranged between 2.5 × 10−9 M (ART‐38) and 8.3 × 10−10 M (OX‐39). Cross inhibition studies revealed that the mAb recognize four different epitopes on the 55‐kDa rat IL 2R subunit.
DOI: 10.4049/jimmunol.131.6.2895
发表时间: 1983-12
影响因子: 4.4
作者:
P. Parham
通讯作者: P. Parham