New candidate

A molecule has been found – a possible "trigger" of multiple sclerosis

Marina Astvatsaturyan, Echo of Moscow

Cells of the immune system of the human body, normally neutralizing bacteria and viruses that enter it, attack their own nervous system with multiple sclerosis. Recently, scientists have managed to identify a previously elusive molecule that can provoke such an attack. This is an autoantigen, or self-antigen, which can point the way to new methods of treating a severe chronic disease. The results of the study are published in the online edition Science Translational Medicine.

The expert of the Science publication German neuroimmunologist Hartmut Wekerle from the Max Planck Institute of Neurobiology in Munich has already called the discovery epoch-making. Scientists have long suspected that autoantigen is an ordinary molecule in the body that the immune system may mistakenly perceive as a threat and trigger the development of multiple sclerosis. As the "main suspect", proteins in the composition of myelin, the sheath that isolates nerves, which is destroyed in patients with multiple sclerosis, were considered.

But years of searching for such a trigger molecule have led to nothing. The new candidate was identified by Swiss immunologists Roland Martin and Mireia Sospedra from The University Hospital of Zurich, which examined the immune T-cells of a patient who died of multiple sclerosis. Usually, T cells are activated when they encounter fragments containing several amino acids of microbes, but the same thing happens to them in people with multiple sclerosis. And Swiss scientists decided to find out which protein fragments stimulate patients' T-cells. To do this, they tested 200 fragment mixtures, each of which had 300 billion varieties.

Two fragments with the most pronounced effect on T cells were found to be part of the enzyme guanosine-diphosphate-L-fucose synthase. It contributes to the modification of sugars in cells involved in various processes from memory formation to blood group determination. T-cells of 12 out of 31 patients with diagnosed multiple sclerosis or early symptoms of the disease reacted to this enzyme.

If the guanosine-diphosphate-L-fucose synthase turns out to be really an autoantigen that triggers the development of multiple sclerosis, then by selecting a dose of this substance, it will be possible to weaken such symptoms of the disease as numbness and muscle weakness, just as allergovaccination prevents an allergic reaction to ragweed pollen, Mireya Sospedra believes. Scientists plan to test this approach on a limited contingent of patients with multiple sclerosis next year.

Article by Jelcic et al. Memory B Cells Activate Brain-Homing, Autoreactive CD4+ T Cells in Multiple Sclerosis is published in the journal Cell.

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