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首页> 外文期刊>Clinical immunology: The official journal of the Clinical Immunology Society >A complement-dependent model of thrombotic thrombocytopenic purpura induced by antibodies reactive with endothelial cells.
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A complement-dependent model of thrombotic thrombocytopenic purpura induced by antibodies reactive with endothelial cells.

机译：与内皮细胞反应的抗体诱导的补体依赖性血栓性血小板减少性紫癜模型。

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Thrombotic thrombocytopenic purpura (TTP) is an immunologically mediated disease characterized by thrombocytopenia, hemolytic anemia, and pathologic changes in various organs, including the kidney, which are secondary to widespread thromboses. Central to TTP is platelet activation, which may occur from a variety of mechanisms, including endothelial cell activation or injury. In this study, injection of K6/1, a monoclonal antibody with widespread reactivity toward endothelia, led to dose-dependent thrombocytopenia in rats. This was magnified if animals were preimmunized with mouse IgG, thereby resulting in an accelerated autologous phase of injury. In this setting, significant anemia also resulted. Rats injected with K6/1 developed renal injury, consisting of tubular damage and glomerular thrombi. Thrombocytopenia and renal morphological abnormalities were eliminated if animals were complement depleted with cobra venom factor prior to K6/1 injection and worsened when the activity of the ubiquitous complement regulator Crry was inhibited with function-neutralizing antibodies. Therefore, we have developed a complement-dependent model of TTP in rats by injecting monoclonal antibodies reactive with endothelial cells. Antibody-directed complement activation leads to stimulation of platelets, through direct interactions with complement fragments and/or indirectly through endothelial cell activation or injury, with the subsequent development of TTP.
机译：血栓性血小板减少性紫癜（TTP）是一种免疫学介导的疾病，其特征是血小板减少症，溶血性贫血和各种器官（包括肾脏）的病理变化是继发于广泛血栓形成的继发因素。 TTP的核心是血小板活化，血小板活化可能是由多种机制引起的，包括内皮细胞活化或损伤。在这项研究中，注射对血管内皮具有广泛反应性的单克隆抗体K6 / 1导致了大鼠的剂量依赖性血小板减少。如果动物用小鼠IgG进行了预免疫，则放大了，从而导致了自体损伤的加速阶段。在这种情况下，还会导致严重的贫血。注射K6 / 1的大鼠出现肾损伤，包括肾小管损伤和肾小球血栓形成。如果在K6 / 1注射前动物补充了眼镜蛇毒因子，使动物的补体消耗减少，则血小板减少症和肾脏形态学异常得以消除;而当泛滥的补体调节因子Crry的活性被功能中和性抗体抑制时，恶化了血小板减少和肾形态异常。因此，我们通过注射与内皮细胞反应的单克隆抗体，在大鼠体内建立了TTP的补体依赖性模型。抗体指导的补体激活通过与补体片段的直接相互作用和/或通过内皮细胞的激活或损伤而间接地导致血小板的刺激，以及随后的TTP的发展。

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