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实验性抗原诱导性关节炎中免疫复合物的捕获机制。

The mechanism of trapping of immune complexes in experimental antigen-induced arthritis.

作者信息

Jasin H E

出版信息

Rheumatology. 1975;6:288-92.

PMID:128111
Abstract

The role of acute inflammation and of specific antibody in the retention of antigen in joint collagenous tissues of immunized rabbits was examined. The role of the acute synovitis occurring immediately after IA antigen injection in the retention of immune complexes was investigated by the concomitant IA injection of trace amounts of 1258-BSA and mono-sodium urate crystals and by the production of an acute Arthus reaction using an unrelated antigen in doubly immunized rabbits. In neither case was more 125I-BSA retained in the inflamed joint tissues compared to the contralateral noninflamed joints 7 days after antigen injection. In addition, immunized rabbits depleted of ciruclating polymorphonuclear leukocytes by previous treatment with nitrogen mustard retained 2.7 times more antigen than control, nonimmune animals. In another experiment, antigen retention in joint collagenous tissues was greatest 30 min after IA injection, before the appearance of acute inflammatory synovitis. These findings suggest that acute inflammation is not a major factor in the retention of antigen in collagenous tissues. To investigate the role of antibody in the retention of antigen, nonimmune rabbits were injected i.v. with purified anti-BSA antibody three days prior to the intraarticular injection of BSA. Over 20 times more antigen was retained irreversibly in collagenous tissues obtained from the injected joints of passively immunized animals as compared to similar tissues of control rabbits. When rabbits were injected i.v. with purified anti-BSA antibody and either killed 20 min or 3 days later, in vitro binding of antigen by joint collagenous tissues was seen only in animals where antibody was allowed to equilibrate with the extravascular space for 3 days. These findings indicate that retention of antigen depends on the presence of extravascular antibody. It is concluded that the trapping of immune complexes in collagenous joint tissues of immunized animals depends on: (1) the presence of antibody in the extravascular space; (2) the diffusion of antigen or soluble complexes into this space; (3) the interaction of antigen or soluble complexes with extravascular antibody with subsequent formation of larger and more insoluble complexes, and (4) the trapping of these complexes in the collagen fiber meshwork.

摘要

研究了急性炎症和特异性抗体在免疫兔关节胶原组织中抗原滞留方面的作用。通过关节内(IA)注射微量125I-牛血清白蛋白(BSA)和尿酸钠晶体,并在双重免疫的兔中使用无关抗原产生急性阿瑟斯反应,研究了IA抗原注射后立即发生的急性滑膜炎在免疫复合物滞留中的作用。在抗原注射7天后,与对侧未发炎关节相比,发炎关节组织中滞留的125I-BSA在这两种情况下均未增多。此外,先前用氮芥处理使循环多形核白细胞耗竭的免疫兔,其滞留的抗原量是对照非免疫动物的2.7倍。在另一项实验中,IA注射后30分钟,即在急性炎症性滑膜炎出现之前,关节胶原组织中的抗原滞留量最大。这些发现表明,急性炎症不是胶原组织中抗原滞留的主要因素。为了研究抗体在抗原滞留中的作用,在关节内注射BSA三天前,给非免疫兔静脉注射纯化的抗BSA抗体。与对照兔的相似组织相比,从被动免疫动物的注射关节获得的胶原组织中不可逆滞留的抗原多20倍以上。当给兔静脉注射纯化的抗BSA抗体,并在20分钟或3天后处死时,仅在抗体与血管外间隙平衡3天的动物中,观察到关节胶原组织对抗原的体外结合。这些发现表明,抗原的滞留取决于血管外抗体的存在。得出的结论是,免疫动物胶原关节组织中免疫复合物的捕获取决于:(1)血管外间隙中抗体的存在;(2)抗原或可溶性复合物扩散到该间隙中;(3)抗原或可溶性复合物与血管外抗体的相互作用,随后形成更大且更不溶性的复合物,以及(4)这些复合物在胶原纤维网中的捕获。

相似文献

1
The mechanism of trapping of immune complexes in experimental antigen-induced arthritis.实验性抗原诱导性关节炎中免疫复合物的捕获机制。
Rheumatology. 1975;6:288-92.
2
Mechanism of trapping of immune complexes in joint collagenous tissues.免疫复合物在关节胶原组织中潴留的机制。
Clin Exp Immunol. 1975 Dec;22(3):473-85.
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The inflammatory role of immune complexes trapped in joint collagenous tissues.被困在关节胶原组织中的免疫复合物的炎症作用。
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Antigen induced arthritis: antigen handling and chronicity of joint inflammation.抗原诱导性关节炎:抗原处理与关节炎症的慢性化
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The specific in vitro antibody-mediated retention of bovine serum albumin by porcine hyaline articular cartilage.猪透明关节软骨对牛血清白蛋白的特异性体外抗体介导保留作用。
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Repair characteristics of the articular cartilage surface following acute inflammatory arthritis.急性炎症性关节炎后关节软骨表面的修复特征
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Arthritis in the rabbit knee joint: a quantitated model.兔膝关节关节炎:一种定量模型。
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Induction of acute and chronic arthritis by intra-articular injection of preformed collagen-anticollagen complexes.通过关节内注射预先形成的胶原蛋白 - 抗胶原蛋白复合物诱导急性和慢性关节炎。
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Electrical charge of the antigen determines intraarticular antigen handling and chronicity of arthritis in mice.抗原的电荷决定了小鼠关节内抗原的处理方式以及关节炎的慢性程度。
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Immune complexes, but not streptococcal cell walls or zymosan, cause chronic arthritis in mouse strains susceptible for collagen type II auto-immune arthritis.免疫复合物而非链球菌细胞壁或酵母聚糖,可在对II型胶原自身免疫性关节炎易感的小鼠品系中引发慢性关节炎。
Cytokine. 1999 Dec;11(12):1046-56. doi: 10.1006/cyto.1999.0503.

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