首页> 外文OA文献 >Mitogenicity and down-regulation of high-affinity interleukin 2 receptor by YTA-1 and YTA-2, monoclonal antibodies that recognize 75-kDa molecules on human large granular lymphocytes.
【2h】

Mitogenicity and down-regulation of high-affinity interleukin 2 receptor by YTA-1 and YTA-2, monoclonal antibodies that recognize 75-kDa molecules on human large granular lymphocytes.

机译:YTA-1和YTA-2是识别人大颗粒淋巴细胞上75 kDa分子的单克隆抗体,它具有高亲和力并下调高亲和性白介素2受体的表达。

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务,本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文,但由于OA文献来源多样且变更频繁,仍可能出现获取不到、文献不完整或与标题不符等情况,如果获取不到我们将提供退款服务。请知悉。

摘要

A large number of interleukin 2 receptors lacking the Tac epitope (IL-2R/p75) were found to be constitutively expressed on the human large granular lymphocyte/natural killer cell line YT, which bears inducible IL-2R/p55 associated with Tac antigen. Two anti-YT IgG1 monoclonal antibodies, YTA-1 and YTA-2, recognizing different epitopes of the same 75- to 80-kDa molecule, were established. The 75-kDa antigen recognized by these monoclonal antibodies was strongly expressed on the large granular lymphocytes of normal peripheral blood mononuclear cells and on various lymphoid cell lines bearing IL-2R/p75. The YTA-1 and YTA-2 antibodies were mitogenic and were different from other mitogenic monoclonal antibodies such as anti-T3 (CD3), anti-T11 (CD2), and KOLT-2 (CD28). Further, they down-regulated the high-affinity IL-2R of peripheral blood mononuclear cells within 24 hr in culture. The relationship between the YTA-1/2 antigen and the IL-2R system is discussed.
机译:发现大量缺乏Tac表位的白介素2受体(IL-2R / p75)在人大颗粒淋巴细胞/天然杀伤细胞系YT上组成性表达,该细胞具有与Tac抗原相关的可诱导IL-2R / p55。建立了两个抗YT IgG1单克隆抗体YTA-1和YTA-2,它们识别相同的75-80kDa分子的不同表位。这些单克隆抗体识别的75 kDa抗原在正常外周血单核细胞的大颗粒淋巴细胞和各种带有IL-2R / p75的淋巴样细胞系中强烈表达。 YTA-1和YTA-2抗体是有丝分裂的,不同于其他有丝分裂的单克隆抗体,例如抗T3(CD3),抗T11(CD2)和KOLT-2(CD28)。此外,他们在培养的24小时内下调了外周血单核细胞的高亲和力IL-2R。讨论了YTA-1 / 2抗原和IL-2R系统之间的关系。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号