首页> 美国卫生研究院文献>Immunology >Evolution of collagen arthritis in mice is arrested by treatment with anti-tumour necrosis factor (TNF) antibody or a recombinant soluble TNF receptor.
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Evolution of collagen arthritis in mice is arrested by treatment with anti-tumour necrosis factor (TNF) antibody or a recombinant soluble TNF receptor.

机译:通过用抗肿瘤坏死因子(TNF)抗体或重组可溶性TNF受体治疗可阻止小鼠胶原关节炎的发展。

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摘要

Immunization of DBA/1 mice with type II collagen within complete Freund's adjuvant leads to arthritis, lasting more than 3 months. Injection of anti-tumour necrosis factor (TNF) IgG, 2 and 3 weeks after immunization prevented the development of arthritis in the following months. This treatment had no effect when started 2 months after induction of the disease. A soluble form of the human recombinant TNF receptor type-beta (rsTNFR-beta), continuously infused at a rate of 20 micrograms/day during the second and third week after immunization, also had a long-term protective effect. Anti-TNF antibody had no effect upon the production of anti-type II collagen antibodies. These results indicate that TNF is critically involved in an early phase of this arthritis.
机译:在完全弗氏佐剂中用II型胶原蛋白对DBA / 1小鼠进行免疫会导致关节炎,持续3个月以上。免疫后2周和3周注射抗肿瘤坏死因子(TNF)IgG可以在接下来的几个月中预防关节炎的发展。诱导该病2个月后开始此治疗无效。在免疫后第二周和第三周以20微克/天的速度连续输注可溶形式的人重组TNF受体β型(rsTNFR-beta),也具有长期保护作用。抗TNF抗体对抗II型胶原蛋白抗体的产生没有影响。这些结果表明TNF严重参与该关节炎的早期阶段。

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