Zheng Biao, Switzer Kirsten, Marinova Ekaterina, Zhang Jinwu, Han Shuhua
Department of Immunology, Baylor College of Medicine, Houston, TX 77030, USA.
Autoimmunity. 2008 Aug;41(5):363-71. doi: 10.1080/08916930801931001.
Copolymer-I (COP-I) is an unique immune regulatory polymer that has been shown to suppress experimental autoimmune encephalomyelitis (EAE) and is a treatment option for multiple sclerosis (MS). To investigate whether its immune suppressive effects can be extended to other autoimmune diseases, we treated mice with COP-I during the induction of collagen-induced arthritis (CIA). Our results show that COP-I treatment exacerbated CIA, leading to faster onset, more severe and longer-lasting disease. The mechanisms underlying the exacerbation of CIA by COP-I treatment include enhanced activation and inflammatory cytokine production by autoreactive T cells and elevated production of autoreactive antibodies. In addition, germinal center response was significantly enhanced by COP-I treatment. Thus, great caution should be taken when COP-I is to be used in MS patients with other autoimmune complications or its potential therapeutic effects are to be extended beyond autoimmune demyelinating diseases.
共聚体-I（COP-I）是一种独特的免疫调节聚合物，已被证明可抑制实验性自身免疫性脑脊髓炎（EAE），是治疗多发性硬化症（MS）的一种选择。为了研究其免疫抑制作用是否能扩展到其他自身免疫性疾病，我们在诱导胶原诱导性关节炎（CIA）期间用COP-I治疗小鼠。我们的结果表明，COP-I治疗使CIA恶化，导致发病更快、病情更严重且持续时间更长。COP-I治疗使CIA恶化的潜在机制包括自身反应性T细胞的激活增强和炎性细胞因子产生增加，以及自身反应性抗体的产生增加。此外，COP-I治疗显著增强了生发中心反应。因此，当COP-I用于患有其他自身免疫并发症的MS患者或其潜在治疗作用要扩展到自身免疫性脱髓鞘疾病以外时，应格外谨慎。
