Myasthenia gravis (MG) is a chronic autoimmune disease in which antibodies block communication between nerves and muscles, leading to skeletal muscle weakness. It can cause double vision, difficulty swallowing, and occasional severe breathing problems, among other issues. Many autoimmune diseases like MG, as well as a number of other human diseases, result from the inability to regulate the activity of IgG antibodies—these diseases are collectively referred to as IgG-mediated pathologies.
In a paper published this month in Cell, researchers at Emory University have discovered a family of enzymes that reduce IgG-mediated pathologies in diseases like MG. The findings, conducted in mouse models, show that a specific enzyme (an endoglycosidase called CU43) was particularly effective in treating diseases caused by overactive antibodies.
The newly discovered enzyme was used to treat a number of different IgG-mediated pathologies in mice and proved to be extremely effective. Compared to drugs currently on the market for treating MG, the new enzyme proved much more effective at alleviating symptoms, and at a much lower dose—it took 4,000 times less enzyme to achieve the same biological effect. For patients, a more effective, lower dose could mean fewer side effects and various options in how the drug is administered.
