Blocking interleukin-23 ameliorates neuromuscular and thymic defects in myasthenia gravis.

Acetylcholine receptor (AChR) myasthenia gravis (MG) is a chronic autoimmune disease characterized by muscle weakness. The AChR autoantibodies are produced by B-cells located in thymic ectopic germinal centers (eGC). No therapeutic approach is curative.