Sakata T, Scudamore R A, Cooke T D
Department of Surgery, Queen's University, Kingston, Ontario, Canada.
Rheumatol Int. 1988;8(2):47-53. doi: 10.1007/BF00271834.
Rabbits were first immunized and later challenged with the same antigen (bovine serum albumin, or ferritin) by injection into the tibialis anterior tendon. Inflammatory changes of the tenosynovium and epitenon included infiltration by neutrophils (early) and mononuclear cells (later) over a 6-week course of tenosynovitis. A pattern of antigen entrapment in the tendon together with immunoglobulin was shown by use of radiolabelled antigen and immunochemical staining. Half-life of antigen in the tissues averaged 5 days over the 6-week period. Changes in the epitenon included cellular necrosis, appearance of phagocytic cells, and disruption of the collagen matrix. Tissues of control animals (challenged without prior immunization) showed minimal changes and significantly less retention of antigen (P greater than 0.005). The model is relevant to the mechanism of tendon damage associated with antigen-driven chronic inflammation, as may be the case in rheumatoid arthritis.
首先对兔子进行免疫,随后通过注射到胫骨前肌腱,用相同抗原(牛血清白蛋白或铁蛋白)进行激发。在为期6周的腱鞘炎病程中,腱鞘和腱外膜的炎症变化包括中性粒细胞浸润(早期)和单核细胞浸润(后期)。通过使用放射性标记抗原和免疫化学染色,显示出抗原与免疫球蛋白一起被困在肌腱中的模式。在6周期间,组织中抗原的半衰期平均为5天。腱外膜的变化包括细胞坏死、吞噬细胞的出现以及胶原基质的破坏。对照动物(未经预先免疫而激发)的组织显示出最小的变化,且抗原保留明显较少(P大于0.005)。该模型与类风湿性关节炎可能出现的与抗原驱动的慢性炎症相关的肌腱损伤机制有关。