Achiron A, Mor F, Margalit R, Cohen I R, Lider O, Miron S
Neuroimmunology Unit, Sheba Medical Center, Tel-Hashomer, Israel.
J Autoimmun. 2000 Nov;15(3):323-30. doi: 10.1006/jaut.2000.0433.
Experimental autoimmune encephalomyelitis (EAE) was induced in Lewis rats either by active immunization with myelin basic protein (MBP) or by adoptive transfer using anti-MBP specific CD4(+)T cells. Treatment with human polyclonal immunoglobulins (IgG) effectively suppressed active EAE. Time-dependent experiments demonstrated that the effect of IgG was manifested only when treatment was given immediately after immunization; administration from day 7 after disease induction did not suppress the disease. In the adoptive transfer model of EAE, IgG had no effect in vivo. However, pretreatment in vitro of the antigen-specific T-cells with IgG inhibited their ability to mediate adoptive EAE, as it did in active EAE. Similarly, in vitro IgG pretreatment of the antigen-specific T-cells suppressed the proliferative response to MBP. Fluorescent Activated Cell Sorter (FACS) analysis demonstrated the binding of IgG to activated T-cell lines that was inhibited by soluble Fc molecules. The differential effects of IgG on active EAE and on the adoptive transfer of EAE suggest that IgG in vivo can suppress disease by acting during the early phase of the immune response which involves naive T cells. The inhibition of T-cell proliferation and adoptive transfer of EAE by incubation of T cells in vitro appears to require higher concentrations of IgG than those obtained in vivo.
实验性自身免疫性脑脊髓炎（EAE）可通过用髓鞘碱性蛋白（MBP）进行主动免疫或使用抗MBP特异性CD4(+)T细胞进行过继转移在Lewis大鼠中诱导产生。用人多克隆免疫球蛋白（IgG）治疗可有效抑制活动性EAE。时间依赖性实验表明，IgG的作用仅在免疫后立即给予治疗时才会显现；在疾病诱导后第7天给药并不能抑制疾病。在EAE的过继转移模型中，IgG在体内没有作用。然而，与在活动性EAE中一样，用IgG在体外预处理抗原特异性T细胞可抑制它们介导过继性EAE的能力。同样，用IgG在体外预处理抗原特异性T细胞可抑制对MBP的增殖反应。荧光激活细胞分选仪（FACS）分析表明，IgG与活化的T细胞系结合，而这种结合可被可溶性Fc分子抑制。IgG对活动性EAE和EAE过继转移的不同作用表明，体内的IgG可通过在涉及初始T细胞的免疫反应早期发挥作用来抑制疾病。通过在体外培养T细胞来抑制T细胞增殖和EAE的过继转移似乎需要比体内获得的浓度更高的IgG。
