Myasthenia gravis (MG) is a chronic autoimmune disorder in which antibodies block communication between nerves and muscle, resulting in weakness of the skeletal muscles. It can cause double vision, difficulty swallowing, and, occasionally, serious breathing difficulties, among other symptoms. Many autoimmune diseases such as MG, as well as a range of other human illnesses, result from the inability to regulate activity of IgG antibodies – collectively, these diseases are referred to as IgG-mediated pathologies.
In a paper out this month in Cell , researchers at Emory University have discovered a family of enzymes that work to reduce IgG-mediated pathologies in diseases like MG. The findings, involving mouse models, show that a specific enzyme (an endoglycosidase called CU43) was particularly effective in treating those diseases caused by overactive antibodies. Human antibodies, although critically important for mounting an immune response to pathogens and fighting disease, sometimes cause disease themselves – including autoimmune diseases.
The enzymes we discovered can modify antibodies in such a way that they no longer cause disease." Eric Sundberg, principal investigator on the study and biochemistry researcher at Emory University's School of Medicine A more effective treatment option The newly discovered enzyme was used to treat a number of different IgG-mediated pathologies in mice and found to be extremely effective. Compared to drugs currently on the market to treat.