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用抗白细胞介素-1抗体调节小鼠关节炎中的软骨破坏。

Modulation of cartilage destruction in murine arthritis with anti-IL-1 antibodies.

作者信息

van de Loo F A, Arntz O J, Otterness I G, van den Berg W B

机构信息

Department of Rheumatology, University Hospital St. Radboud, Nijmegen, The Netherlands.

出版信息

Agents Actions. 1993;39 Spec No:C211-4. doi: 10.1007/BF01972769.

Abstract

One of the early events in murine antigen-induced arthritis is the generation of IL-1 in the inflamed joint. We investigated the role of IL-1 in the acute phase of the arthritic process by selective blockage of IL-1 bioactivity by treatment with neutralizing antibodies. Pretreatment with anti-IL-1 antibodies moderately suppressed joint swelling. The decrease in chondrocyte proteoglycan synthesis seen in the acute phase of arthritis was prevented by treatment with anti-IL-1 antibodies. IL-1 does not appear to be a major contributor to the accelerated breakdown of articular cartilage in this model. The major impact of anti-IL-1 antibodies was the prevention of proteoglycan synthesis inhibition which clearly reduced articular cartilage depletion by maintaining normal proteoglycan synthesis.

摘要

小鼠抗原诱导性关节炎早期事件之一是在炎症关节中产生白细胞介素-1(IL-1)。我们通过用中和抗体处理选择性阻断IL-1生物活性,研究了IL-1在关节炎进程急性期的作用。用抗IL-1抗体预处理可适度抑制关节肿胀。用抗IL-1抗体处理可防止在关节炎急性期观察到的软骨细胞蛋白聚糖合成减少。在该模型中,IL-1似乎不是关节软骨加速破坏的主要因素。抗IL-1抗体的主要作用是防止蛋白聚糖合成受到抑制,通过维持正常的蛋白聚糖合成明显减少了关节软骨损耗。

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