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129/Sv小鼠中抗IgG2a自身抗体的产生:起始于引流肠道的淋巴结,且可通过新生期胸腺切除术预防。

The production of anti-IgG2a autoantibody in the 129/Sv mouse: onset in the lymph nodes draining the intestinal tract and prevention by neonatal thymectomy.

作者信息

Van Snick J L

出版信息

J Immunol. 1981 Mar;126(3):815-8.

PMID:6970221
Abstract

The histological distribution of anti-IgG-secreting cells was studied by measuring the amount of anti-IgG autoantibodies produced in vitro by cells isolated from various lymphoid organs. Before 20 wk, the production of anti-IgG autoantibody in 129/Sv mice from our Institute predominated in the mesenteric and caudal lymph nodes, which both drain the intestinal tract. After 20 wk, the production extended to the spleen and bone marrow. At that time no production was detected in the mediastinal, lumbar, and inguinal lymph nodes. A similar distribution of anti-IgG-secreting cells was observed in 25-wk-old 129/J mice from the Jackson Laboratory. These data indicate that anti-IgG autoimmunity in the 129 primarily results from a local immune response, probably induced by a specific stimulus of intestinal origin. Neonatal thymectomy prevented the production of anti-IgG, demonstrating that the mesenteric anti-IgG production did not result from the direct stimulation of B lymphocytes by endotoxin-like polyclonal activators. It was found that the anti-IgG produced in vitro had the same narrow specificity against IgG2a as its serum counterpart, indicating that this specificity resulted from the selective stimulation of anti-IgG2a-secreting cells rather than from in vivo consumption of anti-IgG antibodies recognizing other IgG subclasses.

摘要

通过测量从各种淋巴器官分离的细胞在体外产生的抗IgG自身抗体的量,研究了抗IgG分泌细胞的组织学分布。在20周龄之前,我们研究所的129/Sv小鼠中抗IgG自身抗体的产生主要集中在肠系膜淋巴结和尾淋巴结,这两个淋巴结都引流肠道。20周龄之后,产生抗体的部位扩展到脾脏和骨髓。此时,在纵隔、腰和腹股沟淋巴结中未检测到抗体产生。在来自杰克逊实验室的25周龄129/J小鼠中观察到了类似的抗IgG分泌细胞分布。这些数据表明,129小鼠中的抗IgG自身免疫主要源于局部免疫反应,可能是由肠道来源的特定刺激诱导的。新生小鼠胸腺切除可阻止抗IgG的产生,这表明肠系膜抗IgG的产生不是由内毒素样多克隆激活剂直接刺激B淋巴细胞所致。研究发现,体外产生的抗IgG与其血清对应物一样,对IgG2a具有相同的狭窄特异性,这表明这种特异性是由抗IgG2a分泌细胞的选择性刺激导致的,而不是由识别其他IgG亚类的抗IgG抗体在体内消耗所致。

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