用单克隆抗γ干扰素抗体抑制和增强大鼠佐剂性关节炎
Suppression and augmentation of rat adjuvant arthritis with monoclonal anti-interferon-gamma antibody.
作者信息
Wiesenberg I, Van der Meide P H, Schellekens H, Alkan S
机构信息
Department of Inflammation/Bone/Allergy, Pharmaceuticals Research Division, Ciba-Geigy, Basle, Switzerland.
出版信息
Clin Exp Immunol. 1989 Nov;78(2):245-9.
Abstract
The effects of a monoclonal antibody (MoAb DB-1), which neutralized rat interferon-gamma (IFN-gamma), on the induction and progression of adjuvant arthritis in Lewis rats induced by intraplantar injection of Freund's complete adjuvant was studied. The animals were treated intraperitoneally with MoAb DB-1 (0.3-5 mg) for various times. Prophylactic treatment with MoAb DB-1, starting 2 days prior to arthritis induction, inhibited oedema in both the injected and non-injected hind paws and delayed joint destruction as shown by radiography. However, despite continued MoAb treatment, the disease progressed. High doses of MoAb DB-1 exacerbated the disease. A control MoAb of the same isotype did not have significant effects on adjuvant arthritis. Therapeutic treatment with the MoAb DB-1 starting 8 days after arthritis induction caused only slight and short-lived inhibitory effects. IFN-gamma appears to be a critical lymphokine for the development of adjuvant arthritis.
摘要
研究了一种中和大鼠γ干扰素（IFN-γ）的单克隆抗体（MoAb DB-1）对足底注射弗氏完全佐剂诱导的Lewis大鼠佐剂性关节炎的诱导和进展的影响。动物腹腔注射不同剂量（0.3 - 5毫克）的MoAb DB-1，持续不同时间。在关节炎诱导前2天开始用MoAb DB-1进行预防性治疗，可抑制注射和未注射后爪的水肿，并通过X射线显示延缓关节破坏。然而，尽管持续进行MoAb治疗，疾病仍在进展。高剂量的MoAb DB-1使疾病恶化。相同亚型的对照单克隆抗体对佐剂性关节炎没有显著影响。在关节炎诱导后8天开始用MoAb DB-1进行治疗性治疗，仅产生轻微且短暂的抑制作用。IFN-γ似乎是佐剂性关节炎发展的关键淋巴因子。
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