Yokochi T, Inoue Y, Fukada M, Kawai M, Yoshikawa K, Suzuki Y, Kato N
Department of Microbiology, Aichi Medical University School of Medicine, Japan.
Autoimmunity. 1991;10(2):125-31. doi: 10.3109/08916939109004816.
Mouse hybridoma cells secreting monoclonal antibody (mAb) against mouse thyroglobulin were established. The implantation of the hybridomas succeeded to induce high titers of circulating mAb against thyroglobulin in sera of mice. By using the implantation of the hybridomas in mice, the effect of autoantibody on the thyroid glands was studied histologically and functionally. In these mice the thyroid follicles were significantly swollen and warped, whereas there was no infiltration of inflammatory cells. The 125I-uptake in their thyroid glands was markedly decreased. There were no functional changes in control mice implanted with non-secreting P3U1 partner cells. Therefore, it was suggested that high titers of anti-thyroglobulin autoantibody could definitely cause the histological and functional damages in the thyroid glands.
建立了分泌抗小鼠甲状腺球蛋白单克隆抗体(mAb)的小鼠杂交瘤细胞。将杂交瘤细胞植入小鼠体内成功诱导出小鼠血清中针对甲状腺球蛋白的高滴度循环单克隆抗体。通过在小鼠体内植入杂交瘤细胞,从组织学和功能上研究了自身抗体对甲状腺的影响。在这些小鼠中,甲状腺滤泡明显肿胀和扭曲,而无炎性细胞浸润。它们甲状腺对125I的摄取明显减少。植入不分泌的P3U1伙伴细胞的对照小鼠无功能变化。因此,提示高滴度的抗甲状腺球蛋白自身抗体肯定能引起甲状腺的组织学和功能损害。