In multiple sclerosis, inflammation in the central nervous system leads to unsheathing of the protective myelin that coats neurons, causing them to degenerate. Scientists have thought that the inflammation is caused by an immune response directed against the myelin. New research lends credence to this belief by revealing certain specifics of how the immune response occurs. The work could help direct future research into therapies for the disease. New research has demonstrated that an immune response against myelin oligodendrocyte glycoprotein is involved in multiple sclerosis. These cultured cells show a control group (top left) and cells expressing the protein (green) at 200x magnification (top right) and at 600x magnification (bottom). Images reprinted with permission of PNAS. Researchers at Heinrich Heine University in Düsseldorf, Philipps University in Marburg and Georg August University in Göttingen, all in Germany, studied the role of antibodies that attack myelin oligodendrocyte glycoprotein, which is embedded in the myelin sheath. Their experiments revealed that these antibodies were circulating in some patients suffering from multiple sclerosis, and they found that cultured cells with the protein on their surface died when exposed to the antibodies. Studies using rats showed that demyelination and neuronal damage occurred in animals exposed to antibodies against the glycoprotein. The work is detailed in a soon-to-be-published PNAS paper (doi/10.1073/pnas.0607242103). In their studies with rats, researchers found that human antibodies directed against myelin oligodendrocyte glycoprotein bind to intact myelin. The left images show rat brain slices that were positive for antibodies against the glycoprotein (shown as green), and the right image shows a slice that was negative for the antibodies. From these findings, the researchers concluded that, in a subgroup of multiple sclerosis patients, antibodies directed against myelin oligodendrocyte glycoprotein caused the neuron damage. Future research will be needed to determine how this immune response relates to clinical and pathological characteristics of the disease and whether an immune response to other proteins also plays a role.