...
首页> 外文期刊>Experimental Biology and Medicine: Journal of the Society for Experimental Biology and Medicine >Immunoglobulin M antiplatelet autoantibodies from mice immunized with rat platelets induce thrombocytopenia and platelet function impairment.
【24h】

Immunoglobulin M antiplatelet autoantibodies from mice immunized with rat platelets induce thrombocytopenia and platelet function impairment.

机译:用大鼠血小板免疫的小鼠的免疫球蛋白M抗血小板自身抗体诱导血小板减少和血小板功能受损。

获取原文
获取原文并翻译 | 示例

摘要

Antiplatelet monoclonal autoantibodies (mAbs) were derived from CBA mice immunized with rat platelets. Two IgM antiplatelet mAbs were further analyzed. L1C43 mAb bound a 150-160 kDa antigen, recognized activated platelets better than resting ones and impaired platelet adhesion, but not clot retraction. L1H31 mAb recognized a +/-95 kDa molecule, bound similarly activated and resting platelets and did not modify platelet adhesion, but inhibited clot retraction. Both mAbs induced in vivo thrombocytopenia most likely through phagocytosis of opsonized platelets. These autoreactive antibodies can thus induce both platelet destruction and impairment of their function. They are reflective of autoantibodies found in human patients and may serve for further analysis of antiplatelet autoantibody pathogenicity and mechanisms of autoimmune disease.
机译:抗血小板单克隆自身抗体(mAb)来源于用大鼠血小板免疫的CBA小鼠。进一步分析了两种IgM抗血小板单克隆抗体。 L1C43 mAb结合了150-160 kDa的抗原,识别的活化血小板比静息的血小板好,并且血小板粘附受损,但不凝结。 L1H31 mAb识别+/- 95 kDa分子,结合相似活化的血小板和静止的血小板,不改变血小板粘附性,但抑制血块回缩。两种单克隆抗体最有可能通过调理血小板的吞噬作用诱导体内血小板减少症。因此,这些自身反应性抗体可以诱导血小板破坏和功能受损。它们反映了人类患者体内发现的自身抗体,可用于进一步分析抗血小板自身抗体的致病性和自身免疫性疾病的机制。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

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