Myasthenia gravis (MG) is an autoimmune disease, meaning the immune system mistakenly attacks the body’s own healthy tissues. In MG, the immune system targets proteins that are essential for communication between nerves and muscles at the neuromuscular junction — the point where nerve cells signal muscles to contract for voluntary movement.

For most people with MG, the immune system produces antibodies against acetylcholine receptors (AChRs). These receptors sit on muscle cells and respond to chemical signals from nerves to trigger muscle contraction. When these receptors are blocked or damaged, muscles cannot contract normally, leading to weakness.

Less commonly, antibodies attack other important proteins involved in nerve-muscle communication, such as muscle-specific kinase (MuSK). About 10% of individuals with MG do not have detectable antibodies to these known targets and are often referred to as “seronegative.”

The exact cause of the autoimmune response in MG is not fully understood. However, abnormalities in the thymus gland — an immune system organ located in the chest — are believed to play a role in many cases by contributing to the production or persistence of harmful antibodies.

MG is generally not considered an inherited disease. While certain genetic factors may increase susceptibility, it does not typically pass directly from parent to child. Some individuals are born with genetic mutations that affect nerve-muscle communication, a condition known as congenital myasthenia. However, congenital myasthenia is a separate and distinct disorder from autoimmune MG.