首页> 外文期刊>Clinical immunology: The official journal of the Clinical Immunology Society >Murine experimental autoimmune gastritis models refractive to development of intrinsic factor autoantibodies, cobalamin deficiency and pernicious anemia.
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Murine experimental autoimmune gastritis models refractive to development of intrinsic factor autoantibodies, cobalamin deficiency and pernicious anemia.

机译:小鼠实验性自身免疫性胃炎模型可抵抗内在因素自身抗体,钴胺素缺乏症和恶性贫血的发展。

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Researchers have developed murine lymphopenic, non-lymphopenic, transgenic, spontaneous and infectious agent based models to induce an experimental autoimmune gastritis (EAG) for the study of human organ-specific autoimmune disease. These models result in a chronic inflammatory mononuclear cell infiltrate in the gastric mucosa, destruction of parietal and zymogenic cells with autoantibodies reactive to the gastric parietal cells and the gastric H+/K+ ATPase (ATP4), arguably hallmarks of a human autoimmune gastritis (AIG). In the case of AIG, it is well documented that, in addition to parietal cell antibodies being detected in up to 90% of patients, up to 70% have intrinsic factor antibodies with the later antibodies considered highly specific to patients with pernicious anemia. This is the first report specifically investigating the occurrence of intrinsic factor antibodies, cobalamin deficiency and pernicious anemia in EAG models. We conclude, in contrast to AIG, that, in the three EAG models examined, intrinsic factor is not selected as a critical autoantigen.
机译:研究人员已经开发出基于小鼠淋巴细胞减少,非淋巴细胞减少,转基因,自发和感染性因子的模型,以诱导实验性自身免疫性胃炎(EAG),用于研究人体器官特异性自身免疫性疾病。这些模型导致慢性炎性单核细胞浸润到胃粘膜中,破坏具有对胃壁细胞和胃H + / K + ATPase(ATP4)反应性的自身抗体的壁细胞和产酶细胞,可以说是人类自身免疫性胃炎(AIG)的标志。对于AIG,有充分的文献记载,除了在多达90%的患者中检测到壁细胞抗体外,多达70%的患者还具有内在因子抗体,而后来的抗体被认为对恶性贫血患者具有高度特异性。这是第一份专门调查EAG模型中内在因子抗体,钴胺素缺乏症和恶性贫血的发生的报告。与AIG相比,我们得出的结论是,在所检查的三个EAG模型中,没有选择内在因素作为关键的自身抗原。

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