Garred P, Michaelsen T E, Aase A
Institute of Immunology and Rheumatology, National Hospital, Oslo, Norway.
Scand J Immunol. 1989 Sep;30(3):379-82. doi: 10.1111/j.1365-3083.1989.tb01225.x.
Using a matched series of human-mouse chimaeric IgG anti-5-iodo-4-hydroxy-3-nitrophenacetyl (anti-NIP) antibodies and NIP-bovine serum albumin (NIP-BSA) we examined how different variables influence the activation pattern of complement. When BSA was used with different hapten densities and the input of NIP-BSA was altered, we observed a change in the subclass reaction pattern. IgG3 fixed more Clq than IgG1 and IgG2 in all situations. IgG1 was slightly better than IgG3 and IgG2 at high antigen concentrations at activating C4 and C3 and inducing formation of the terminal complement complex (TCC). When the epitope density and/or the NIP-BSA concentration was reduced, IgG3 became best, followed by IgG1 and IgG2. IgG1 now revealed a marked prozone. Furthermore, IgG4 was found to activate C3 and mediate TCC formation at high epitope and complement concentrations.
我们使用一系列匹配的人-鼠嵌合IgG抗5-碘-4-羟基-3-硝基苯乙酰（抗-NIP）抗体和NIP-牛血清白蛋白（NIP-BSA），研究了不同变量如何影响补体的激活模式。当使用具有不同半抗原密度的BSA并改变NIP-BSA的输入量时，我们观察到亚类反应模式发生了变化。在所有情况下，IgG3比IgG1和IgG2结合更多的Clq。在高抗原浓度下激活C4和C3以及诱导末端补体复合物（TCC）形成时，IgG1略优于IgG3和IgG2。当表位密度和/或NIP-BSA浓度降低时，IgG3表现最佳，其次是IgG1和IgG2。此时IgG1出现明显的前带现象。此外，发现IgG4在高表位和补体浓度下激活C3并介导TCC形成。
