Yoshino S
Department of Microbiology, Saga Medical School, Japan.
Immunopharmacology. 1995 Nov;31(1):103-8. doi: 10.1016/0162-3109(95)00038-5.
We previously demonstrated that intra-articular injection of silicone in rats induced acute arthritis followed by chronic destructive joint inflammation in which T cells played a role. To investigate whether the model of T cell-mediated chronic silicone-induced arthritis (SIA) is modified by oral administration of type II collagen (CII), rats were fed CII either before or after intra-articular injection of silicone. We found that feeding CII either before or after intra-articular injection of silicone markedly suppressed the development of chronic arthritis. The early phase of acute joint inflammation was not affected by the oral antigen. There were no proliferative responses to CII of lymph node cells from rats with SIA. The proliferation to CII of lymph node cells from CII-primed rats was markedly suppressed by the addition of spleen cells from animals fed CII. Furthermore, the proliferative response to keyhole limpet hemocyanin (KLH) of KLH-sensitized lymph node cells was also suppressed by the addition of CII plus spleen cells from CII-fed animals. Injection of the spleen cells into rats followed by intra-articular injection of silicone inhibited the development of chronic SIA. These results indicate that T cell-mediated chronic arthritis may be downregulated by oral administration of CII and that the downregulation of joint inflammation may be due to the generation of CII-specific regulatory lymphocytes that react to CII abundant in cartilage.
我们先前证明，向大鼠关节腔内注射硅酮会引发急性关节炎，随后导致慢性破坏性关节炎症，其中T细胞发挥了作用。为了研究口服II型胶原蛋白（CII）是否会改变T细胞介导的慢性硅酮诱导性关节炎（SIA）模型，在向大鼠关节腔内注射硅酮之前或之后给它们喂食CII。我们发现，在关节腔内注射硅酮之前或之后喂食CII均能显著抑制慢性关节炎的发展。急性关节炎症的早期阶段不受口服抗原的影响。SIA大鼠的淋巴结细胞对CII没有增殖反应。添加来自喂食CII动物的脾细胞后，CII致敏大鼠的淋巴结细胞对CII的增殖明显受到抑制。此外，添加CII和来自喂食CII动物的脾细胞也会抑制匙孔血蓝蛋白（KLH）致敏的淋巴结细胞对KLH的增殖反应。向大鼠注射脾细胞，随后关节腔内注射硅酮，可抑制慢性SIA的发展。这些结果表明，口服CII可能会下调T细胞介导的慢性关节炎，关节炎症的下调可能是由于产生了对软骨中大量存在的CII起反应的CII特异性调节淋巴细胞。
