Marta Cecilia B, Bansal Rashmi, Pfeiffer Steven E
Department of Neuroscience, University of Connecticut Medical School, Farmington, CT 06030-3401, United States.
J Neuroimmunol. 2008 May 30;196(1-2):35-40. doi: 10.1016/j.jneuroim.2008.02.002. Epub 2008 Apr 11.
Antibodies to myelin oligodendrocyte glycoprotein (MOG) have been implicated in Multiple Sclerosis demyelination through activation of complement and/or macrophage-effector processes. We presented a novel mechanism, whereby MOG on oligodendrocytes, when cross-linked with anti-MOG and secondary antibody resulted in its repartitioning into lipid rafts, and changes in protein phosphorylation and morphology. Here, we show that similar events occur when anti-MOG is cross-linked with Fc receptors (FcRs) present on microglia but not with complement. These results indicate that FcRs are endogenous antigen/antibody cross-linkers in vitro, suggesting that FcRs could be physiologically relevant in vivo and possible targets for therapy in Multiple Sclerosis.
髓鞘少突胶质细胞糖蛋白（MOG）抗体通过补体激活和/或巨噬细胞效应过程参与了多发性硬化症的脱髓鞘病变。我们提出了一种新机制，即少突胶质细胞上的MOG与抗MOG和二抗交联后，会重新分配到脂筏中，并导致蛋白质磷酸化和形态发生变化。在此，我们表明，当抗MOG与小胶质细胞上存在的Fc受体（FcRs）交联而非与补体交联时，会发生类似事件。这些结果表明，FcRs在体外是内源性抗原/抗体交联剂，提示FcRs在体内可能具有生理相关性，并且可能是多发性硬化症治疗的潜在靶点。
