The medication efgartigimod, which is already used to treat myasthenia gravis (MG), may do more than lower harmful autoantibodies: It may also help restore balance among different immune cells in the body, according to a recent study published in Neurology Neuroimmunology & Neuroinflammation.
In MG, the immune system interferes with communication between nerves and muscles. This disruption causes weaker muscle contractions, leading to symptoms such as muscle weakness, drooping eyelids and fatigue.
Until now, doctors knew that efgartigimod works by blocking a protein called FcRn. Normally, FcRn helps antibodies (proteins made by the immune system) stay in the body longer. By blocking FcRn, efgartigimod reduces the total number of antibodies, including harmful autoantibodies that mistakenly attack the body’s own tissues.
In this new study involving nine MG patients, researchers found something unexpected: Efgartigimod increased a type of immune cell called plasma cells, which usually produce antibodies. These plasma cells were not harmful — instead, they seemed to calm down the overactive immune system.
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After treatment with efgartigimod, patients showed increases in both plasma cells and memory B cells, a type of white blood cell. The rise in plasma cells was linked to improvements in muscle strength test scores, suggesting a direct connection between these immune changes and symptom relief.
This finding is important because it reveals another way efgartigimod may help people with MG: not only by reducing harmful antibodies, but also by promoting immune balance.
“A deep understanding of the immunologic effects of efgartigimod can help to optimize its usage over time in individual patients,” the researchers said. Knowing exactly how the therapy works could also help doctors monitor how well a patient is responding to treatment over time.
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