Poston R N
Lancet. 1984 Jun 9;1(8389):1268-71. doi: 10.1016/s0140-6736(84)92448-6.
Heat-aggregated immunoglobulin G ( HAGG ) bound avidly to solid-phase basic proteins, including myelin basic protein. In contrast, monomeric immunoglobulin bound weakly. Bound HAGG could activate complement. Normal human serum strongly inhibited the binding of HAGG , even when decomplemented or greatly diluted. Cerebrospinal fluid was also inhibitory, but the effect was weaker. Apart from inhibition by decomplemented serum, the biochemical characteristics of the interaction were similar to those of other Fc ligands with IgG, particularly C1q. In multiple sclerosis this interaction could occur between IgG and central-nervous-system myelin basic protein, leading to demyelination by activation of immune mechanisms of tissue damage. Bound IgG is present in multiple sclerosis plaques and IgG from multiple sclerosis patients can produce demyelination in experimental models. However, there is little evidence of any specific immunity to central-nervous-system antigens in multiple sclerosis, and this non-specific interaction might be an important link in the pathogenesis of the disorder.
热聚集免疫球蛋白G（HAGG）能与包括髓鞘碱性蛋白在内的固相碱性蛋白紧密结合。相比之下，单体免疫球蛋白的结合较弱。结合的HAGG可激活补体。正常人血清能强烈抑制HAGG的结合，即使血清补体已去除或被大量稀释。脑脊液也有抑制作用，但效果较弱。除了补体去除血清的抑制作用外，这种相互作用的生化特性与其他与IgG相互作用的Fc配体（特别是C1q）相似。在多发性硬化症中，这种相互作用可能发生在IgG与中枢神经系统髓鞘碱性蛋白之间，通过激活组织损伤的免疫机制导致脱髓鞘。结合的IgG存在于多发性硬化症斑块中，来自多发性硬化症患者的IgG可在实验模型中导致脱髓鞘。然而，几乎没有证据表明在多发性硬化症中存在针对中枢神经系统抗原的任何特异性免疫，这种非特异性相互作用可能是该疾病发病机制中的一个重要环节。
