When someone has multiple sclerosis (MS), their immune cells target the nervous system instead of the intruding bacteria and viruses. For a long time, it had been suspected that a self-antigen—a normal molecule in the body that the immune system mistakenly treats as a threat—can trigger MS. Researchers had suspected them to be the proteins in myelin – the nerve insulation that erodes in patients with the disease.
Yet, after years of searching, the molecule responsible still couldn’t be found… until now. The long-sought out molecule that provokes these immune attacks called a self-antigen may have finally been pinpointed by researchers, thus exposing a way towards potential treatments. “The work is monumental, and it’s tantalizing,” said neuroimmunologist Hartmut Wekerle of the Max Planck Institute of Neurobiology in Munich, Germany, who wasn’t connected to the study.
The researchers responsible for finding the molecule are immunologists Roland Martin and Mireia Sospedra of University Hospital of Zurich in Switzerland and their colleagues. They found it because they decided to research whether there were other candidates, other possible molecules apart from the expected. To do this they analyzed immune cells known as T cells that came from a patient who died from MS. T cells normally switch on when they encounter protein fragments containing just a few amino acids that belong to an invading microbe. However, they also turn on in people who have MS.
The team tested 200 fragment mixtures, each containing 300 billion varieties of protein shards. They wanted to determine which ones stimulated the patients’ T cells. The two fragments with the strongest effect turned out to be part of a human enzyme called guanosine diphosphate-L-fucose synthase. This enzyme is the one which helps cells remodel sugars that are involved in everything from laying down memories to determining our blood type.
The study also found that T cells from 12 of 31 patients who either had been diagnosed with MS or had shown early symptoms of the disease also reacted to the enzyme. In addition, T cells from four of the eight patients tested responded to a bacterial version of the enzyme—lending credence to the recently proposed idea that intestinal bacteria may help spark the disease. Although, according to immunologist Ashutosh Mangalam of The University of Iowa in Iowa City says, “The gut microbiome angle is a bit of a stretch” because some of the bacteria that produce the enzyme are less abundant in MS patients than in healthy people.
Regardless, the fact remains that even though guanosine diphosphate-L-fucose synthase is prevalent in the brain, “it has never been a candidate in the past,” says neuroimmunologist Reinhard Hohlfeld of Ludwig Maximilians University in Munich. The discovery, he says, is “a first step in an interesting new direction.” The research has been published in Science Translational Medicine.
If guanosine diphosphate-L-fucose synthase does turn out to be one of the elusive MS self-antigens, it would be possible to dose patients with it. Such a treatment might tame symptoms such as numbness and muscle weakness in much the same way that allergy shots prevent people from reacting to substances like ragweed pollen for example. Sospedra and her colleagues plan to start testing this strategy with MS patients next year.
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