Efgartigimod, a medicine designed to lower harmful antibodies in the body, restored muscle strength and helped rebalance immune cell numbers in mice with myasthenia gravis (MG), according to a recent study published in International Immunopharmacology.
In MG the immune system mistakenly attacks acetylcholine receptors (AChR), which are essential for transmitting signals from nerves to muscles. By producing anti-AChR antibodies, the immune system disrupts communication between nerves and muscles, leading to weakened muscle contractions and symptoms such as muscle weakness and fatigue.
In this study, researchers created MG symptoms in mice by injecting them with a small piece of the AChR protein. The mice lost weight, grew weaker and developed higher levels of anti-AChR antibodies, mimicking how the disease happens in humans. Then, the researchers gave some of these mice weekly injections of efgartigimod, a drug that reduces levels of anti-AChR antibodies in the bloodstream.
Mice treated with efgartigimod regained muscle strength, recovered lost weight and had lower levels of the harmful antibodies compared to untreated mice.
“The observed improvements in clinical symptoms and immunological parameters support the potential clinical utility of this therapeutic approach,” the researchers said.
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The researchers also looked at special immune cells called dendritic cells (DCs). In mice with MG, the balance of these cells was off: one type (called cDC1) was too common, while another type (cDC2) was lacking. This imbalance could be part of what drives MG. Mice treated with efgartigimod showed a return to a more balanced mix of these cells, suggesting that efgartigimod works in two ways: it reduces harmful antibodies and it also restores balance in the quantity of different immune cells.
While these findings are promising, the researchers caution that more studies are needed to fully understand how efgartigimod affects immune cells over time and how that relates to MG symptoms and treatment success.
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