Wilder R L, Calandra G B, Garvin A J, Wright K D, Hansen C T
Arthritis Rheum. 1982 Sep;25(9):1064-72. doi: 10.1002/art.1780250906.
Sixteen inbred rat strains were examined for susceptibility and resistance to group A streptococcal cell wall-induced polyarthritis. The findings indicated that 2 or more genetic loci, as well as sex-related factors, played a major role in determining susceptibility to arthritis in this model. Breeding studies demonstrated that susceptibility was a dominant or codominant trait. A positive association between the severity of arthritis and the development of chronic inflammation in multiple tissues was also observed. In strains that were relatively resistant to arthritis, chronic inflammation was generally limited to the spleen. Since translocation of the poorly degradable and phlogogenic streptococcal cell walls to the synovium and other tissues appears to initiate inflammation, these studies suggested that susceptibility might be the result of a defect in host mechanisms limiting cell wall dissemination.
对16种近交系大鼠进行了A组链球菌细胞壁诱导的多关节炎易感性和抗性检测。结果表明,在该模型中,2个或更多的基因位点以及性别相关因素在决定关节炎易感性方面起主要作用。育种研究表明,易感性是显性或共显性性状。还观察到关节炎严重程度与多个组织中慢性炎症发展之间存在正相关。在对关节炎相对抗性的品系中,慢性炎症通常局限于脾脏。由于难以降解且具有致炎作用的链球菌细胞壁向滑膜和其他组织的转移似乎引发了炎症,这些研究表明,易感性可能是宿主限制细胞壁扩散机制缺陷的结果。