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首页> 外文期刊>Journal of molecular medicine: Official organ of the "Gesellschaft Deutscher Naturforscher und Arzte." >Injection of celiac disease patient sera or immunoglobulins to mice reproduces a condition mimicking early developing celiac disease
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Injection of celiac disease patient sera or immunoglobulins to mice reproduces a condition mimicking early developing celiac disease

机译:向小鼠注射腹腔疾病患者的血清或免疫球蛋白可模仿早期发展的腹腔疾病

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Typical features of celiac disease are small-bowel villus atrophy, crypt hyperplasia, and inflammation which develop gradually concomitant with ingestion of gluten. In addition, patients have anti-transglutaminase 2 (TG2) autoantibodies in their serum and tissues. The aim of this study was to establish whether celiac disease can be passively transferred to mice by serum or immunoglobulins. Serum aliquots or purified immunoglobulins (Ig) were intraperitoneally injected into Hsd:Athymic Nude-Foxn1nu mice for 8 or 27 days. As mice do not have proper IgA transport from peritoneum to blood, sera with a high content of IgG class anti-TG2 antibodies from untreated IgA-deficient celiac patients were used. Mouse sera were tested for celiac disease-specific autoantibodies, and several tissues were analyzed for autoantibody deposits targeted to TG2. Morphological assessment was made of the murine small intestinal mucosa. Injection of celiac disease patient sera or total IgG led to a significant delay in weight gain and mild diarrhea in a subset of mice. The mice injected with celiac patient sera or IgG had significantly decreased villus height crypt depth (Vh/CrD) ratios and celiac disease-specific autoantibody deposits targeted to TG2 in several tissues, including the small intestine. None of these features were observed in control mice. We conclude that administration of IgA-deficient celiac disease patient serum or total IgG induces both deterioration of the intestinal mucosa and clinical features of celiac disease in mice. The experimentally induced condition in the mice injected with patient serum or IgG resembles early developing celiac disease in humans.
机译:乳糜泻的典型特征是小肠绒毛萎缩,隐窝增生和发炎,随着面筋的摄入逐渐发炎。此外,患者的血清和组织中具有抗转谷氨酰胺酶2(TG2)自身抗体。这项研究的目的是确定乳糜泻是否可以通过血清或免疫球蛋白被动转移给小鼠。将血清等分试样或纯化的免疫球蛋白(Ig)腹膜内注射到Hsd:Athymic Nude-Foxn1nu小鼠中8或27天。由于小鼠没有从腹膜到血液的适当IgA转运,因此使用了来自未经治疗的IgA缺陷型腹腔患者的高含量IgG类抗TG2抗体的血清。测试小鼠血清的乳糜泻特异性自身抗体,并分析几种组织的靶向TG2的自身抗体沉积物。对小鼠小肠粘膜进行形态学评估。腹腔疾病患者血清或总IgG的注射导致部分小鼠体重增加显着延迟和轻度腹泻。注射了腹腔患者血清或IgG的小鼠的绒毛高度隐窝深度(Vh / CrD)比和针对TG2的腹腔疾病特异性自身抗体沉积物在包括小肠在内的几种组织中均有明显降低。在对照小鼠中没有观察到这些特征。我们得出的结论是,给予IgA缺陷的腹腔疾病患者血清或总IgG会诱发小鼠肠粘膜的恶化和腹腔疾病的临床特征。注射了患者血清或IgG的小鼠中实验诱导的疾病类似于人类早期发展的乳糜泻。

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