• 主题
高级搜索  >
历史搜索 清空历史
首页> 美国卫生研究院文献>The Journal of Experimental Medicine >Tumor dormancy and cell signaling. II. Antibody as an agonist in inducing dormancy of a B cell lymphoma in SCID mice
【2h】

Tumor dormancy and cell signaling. II. Antibody as an agonist in inducing dormancy of a B cell lymphoma in SCID mice

机译：肿瘤休眠和细胞信号传导。二。抗体作为诱导SCID小鼠B细胞淋巴瘤休眠的激动剂

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。
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Tumor dormancy can be induced in a murine B cell lymphoma (BCL1) by immunizing BALB/c mice with the tumor immunoglobulin (Ig) before tumor cell challenge. In this report, we have investigated the immunological and cellular mechanisms underlying the induction of dormancy. BCL1 tumor cells were injected into SCID mice passively immunized with antibody against different epitopes on IgM or IgD with or without idiotype (Id)-immune T lymphocytes. Results indicate that antibody to IgM is sufficient to induce a state of dormancy. Antibodies against other cell surface molecules including IgD and CD44 (Pgp1) had no effect on tumor growth. Id-immune T cells by themselves also had no effect on tumor growth in SCID mice. However, simultaneous transfer of anti-Id and Id-immune T cells enhanced both the induction and duration of the dormant state. In vitro studies indicated that antibody to IgM induced apoptosis within several hours and cell cycle arrest by 24 h. Hyper cross-linking increased apoptosis. The Fc gamma RII receptor played little or no role in the negative signaling. Antibodies that did not negatively signal in vitro did not induce dormancy in vivo. The results suggest that anti-IgM plays a decisive role in inducing tumor dormancy to BCL1 by acting as an agonist of IgM-mediated signal transduction pathways.
机译：通过在肿瘤细胞攻击前用肿瘤免疫球蛋白（Ig）免疫BALB / c小鼠，可以在鼠B细胞淋巴瘤（BCL1）中诱导肿瘤休眠。在本报告中，我们研究了诱导休眠的免疫学和细胞机制。将BCL1肿瘤细胞注射到用抗IgM或IgD上具有或不具有独特型（Id）免疫T淋巴细胞的不同表位的抗体被动免疫的SCID小鼠中。结果表明，针对IgM的抗体足以诱导休眠状态。针对其他细胞表面分子（包括IgD和CD44（Pgp1））的抗体对肿瘤生长没有影响。自身免疫Id的T细胞也对SCID小鼠的肿瘤生长没有影响。然而，抗Id和Id免疫T细胞的同时转移增强了休眠状态的诱导和持续时间。体外研究表明，抗IgM的抗体可在数小时内诱导细胞凋亡，并在24小时内诱导细胞周期停滞。过度交联增加细胞凋亡。 FcγRII受体在阴性信号中几乎没有作用。在体外不产生负面信号的抗体不会在体内诱导休眠。结果表明，抗IgM通过充当IgM介导的信号转导途径的激动剂，在诱导BCL1的肿瘤休眠中起决定性作用。

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