Greenblatt J J, Hunter N, Schwab J H
Clin Exp Immunol. 1980 Dec;42(3):450-7.
The antibody response to group A streptococcal cell wall components was measured in rats during the development of chronic, remittent experimental arthritis. The arthritis was induced by a single intraperitoneal injection of an aqueous suspension of group A streptococcal cell wall fragments and antibodies were measured by a radioactive antigen-binding assay. Antibodies in serum against both peptidoglycan and A polysaccharide reached maximum levels at 1 or 2 weeks and declined to preimmunization levels by day 63. The kinetics and magnitude of the antibody responses were similar in neonatally thymectomized and non-thymectomized rats. A relationship between chronic joint lesions and anti-peptidoglycan concentration in serum was indicated, since all rats which produced high levels of antibody developed severe chronic arthritis. However, 46% of the rats which produced very low levels of antibody also developed moderate to severe arthritis. There was no correlation between anti-A polysaccharide antibodies and joint disease, although the concentration of this antibody was 10- to 100-fold greater than the anti-peptidoglycan. We conclude that antibody can be a component in the pathogenesis of this experimental model of arthritis, but its role requires further elucidation.
在慢性、缓解性实验性关节炎的发展过程中,对大鼠体内针对A组链球菌细胞壁成分的抗体反应进行了测量。通过单次腹腔注射A组链球菌细胞壁片段的水悬浮液诱导关节炎,并通过放射性抗原结合试验测量抗体。血清中针对肽聚糖和A多糖的抗体在1或2周时达到最高水平,并在第63天时降至免疫前水平。新生期胸腺切除和未胸腺切除的大鼠中,抗体反应的动力学和幅度相似。血清中慢性关节病变与抗肽聚糖浓度之间存在关联,因为所有产生高水平抗体的大鼠都发展为严重的慢性关节炎。然而,46%产生极低水平抗体的大鼠也发展为中度至重度关节炎。尽管抗A多糖抗体的浓度比抗肽聚糖高10至100倍,但抗A多糖抗体与关节疾病之间没有相关性。我们得出结论,抗体可能是这种实验性关节炎模型发病机制的一个组成部分,但其作用需要进一步阐明。