Herman J H, Herzig E B, Crissman J D, Dennis M V, Hess E V
J Rheumatol. 1980 Sep-Oct;7(5):694-705.
Investigations were performed to determine the potential of an immunologically-mediated basis underlying development of severe bilateral knee chondrolysis arising over a 2-yr period in a 29-yr-old man. Humoral and cell-mediated immune responses to autologous and homologous articular cartilage proteoglycan and collagen rich fractions were identified in sequential studies. Employing gradient derived peripheral blood mononuclear cells there was demonstration of spontaneous, T cell mitogen augmented and autologous cartilage antigen-induced release of factors capable of degrading articular cartilage proteoglycans and inhibiting chondrocyte glycosaminoglycan synthesis. Evidence has thus been provided incriminating immunologic events, likely functioning in a perpetuant manner, in the pathogenesis of this chondrolytic process.
进行了相关研究,以确定一名29岁男性在2年时间里出现严重双侧膝关节软骨溶解症的潜在免疫介导基础。在一系列研究中,确定了对自体和同源关节软骨蛋白聚糖及富含胶原蛋白部分的体液免疫和细胞介导免疫反应。利用梯度分离的外周血单核细胞,证实了自发的、T细胞丝裂原增强的以及自体软骨抗原诱导的能够降解关节软骨蛋白聚糖并抑制软骨细胞糖胺聚糖合成的因子释放。因此,已有证据表明免疫事件在这一软骨溶解过程的发病机制中起作用,且可能以持续的方式发挥作用。