VARIOUS EXPRESSIONS OF A UNIQUE ANTI-HUMAN THYROGLOBULIN ANTIBODY REPERTOIRE IN NORMAL STATE AND AUTOIMMUNE-DISEASE
VARIOUS EXPRESSIONS OF A UNIQUE ANTI-HUMAN THYROGLOBULIN ANTIBODY REPERTOIRE IN NORMAL STATE AND AUTOIMMUNE-DISEASE
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DOI：
10.1002/eji.1830150311
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发表时间：
1985-01-01
影响因子：
5.4
通讯作者：
LISSITZKY, S
中科院分区：
文献类型：
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作者：
RUF, J;CARAYON, P;LISSITZKY, S
用人甲状腺球蛋白（hTgb）免疫家兔、正常人、Graves病、桥本甲状腺炎和甲状腺癌患者，制备了多克隆hTgb抗体。各种Ab制剂对hTgb的亲合力范围为0.3 × 10 - 6。1010-2.2 ×1010 M-1通过使用经过充分表征的针对hTgb的小鼠单克隆抗体（mAb），结果表明，兔中诱导的抗hTgb Ab、正常人中的天然Ab和疾病患者中的自身抗体的良好特异性相似;但它们与兔抗牛和抗猪甲状腺球蛋白Ab的特异性不同，兔抗牛和抗猪甲状腺球蛋白Ab只能抑制少数mAb的hTgb结合。兔和甲状腺癌患者的抗hTgb抗体与正常人的抗hTgb抗体仅一致升高。Graves病和桥本氏甲状腺炎患者显示浓度增加，主要限于与mAb识别的少数抗原决定簇反应的Ab。显然，抗hTgb Ab的库在小鼠、兔和人中是相似的。在正常和病理条件下抗hTgb Ab的相同精细特异性的发现意味着自身抗体在正常受试者中产生，并且通过调节过程保持在低水平，所述调节过程在自身免疫性疾病中对于所选表位失败。
Polyclonal anti-human thyroglobulin (hTgb) antibodies (Ab) were purified from sera of rabbits immunized with human thyroglobulin, normal humans and patients suffering from Graves'' disease, Hashimoto''s thyroiditis and thyroid carcinoma. The avidity of the various Ab preparations for hTgb ranged from 0.3 .times. 1010-2.2 .times. 1010 M-1. By using well characterized mouse monoclonal antibodies (mAb) directed against hTgb, it was shown that the fine specificities of induced anti-hTgb Ab in rabbits, natural Ab in normal subjects and autoantibodies in diseased patients were similar; however, they differed from that of rabbit anti-bovine and anti-porcine thyroglobulin Ab which were able to inhibit the hTgb binding of only a few of the mAb. Anti-hTgb in rabbits and in patients with thyroid carcinoma varied from those in normal subjects only by uniformly elevated serum titers. Patients with Graves'' disease and Hashimoto''s thyroiditis showed an increased concentration essentially restricted to Ab reacting with few of the antigenic determinants recognized by the mAb. Evidently, the repertoire of anti-hTgb Ab is similar in mouse, rabbit and human. The finding of identical fine specificities for anti-hTgb Ab in normal and pathological conditions implies that autoantibodies are produced in normal subjects and held to a low level by regulatory processes which fail with respect to selected epitopes in autoimmune diseases.