Fujita M
Section of Pathology, Institute of Immunological Science, Hokkaido University, Sapporo, Japan.
Hokkaido Igaku Zasshi. 1988 May;63(3):415-24.
Pathogenesis and regulation of type II collagen (IIC) induced arthritis (CA) were investigated in mice system. CA could be successfully induced in hundred percent female mice of DBA/1J strain following immunization by an intradermal injection with emulsion of bovine IIC plus Freund's complete adjuvant into the tail base and a subsequent challenge injection with IIC in saline in the same place. The incidence and severity of the CA were suppressed by an intraperitoneal injection with a mouse gamma-globulin: histamine conjugate. On the other hand, neither histamine nor mouse gamma-globulin alone showed no suppressive effect and the former markedly accelerated the onset of the CA and augmented the severity. Next, we analyzed incidence of CA in allogeneic bone marrow chimeras prepared by using the combination of DBA/1J (H-2q, Igh-1c, Hc1) and SWR/J (H-2q, Igh-1c, Hco) mice the latter of which are unable to generate CA. As previously described, only chimeras where DBA/1J were used as recipient of bone marrow showed complement 5 (C5) in sera. Further, CA incidence was quite high (90%) in such chimeras. By contrast, none of chimeric mice where SWR/J were used as recipient showed serum C5 and CA. The result of chimera experiments indicated that C5 level in sera was one of the determinants in CA induction and that lymphoid cells of SWR/J mice themselves had no deficiency in inducing the CA.
在小鼠系统中研究了II型胶原(IIC)诱导的关节炎(CA)的发病机制和调控。通过将牛IIC与弗氏完全佐剂的乳剂皮内注射到DBA/1J品系的雌性小鼠尾基部进行免疫,随后在同一部位用生理盐水配制的IIC进行激发注射,可在100%的该品系雌性小鼠中成功诱导出CA。腹腔注射小鼠γ-球蛋白:组胺缀合物可抑制CA的发病率和严重程度。另一方面,单独的组胺或小鼠γ-球蛋白均未显示出抑制作用,且前者显著加速了CA的发病并加重了严重程度。接下来,我们分析了使用DBA/1J(H-2q,Igh-1c,Hc1)和SWR/J(H-2q,Igh-1c,Hco)小鼠组合制备的同种异体骨髓嵌合体中CA的发病率,后者无法诱发CA。如前所述,只有以DBA/1J作为骨髓受体的嵌合体血清中显示有补体5(C5)。此外,此类嵌合体中CA的发病率相当高(90%)。相比之下,以SWR/J作为受体的嵌合小鼠均未显示血清C5和CA。嵌合体实验结果表明,血清中的C5水平是CA诱导的决定因素之一,且SWR/J小鼠自身的淋巴细胞在诱导CA方面没有缺陷。