Immunopathology of Myasthenia Gravis

The thymus gland plays a central role in the development of AChR-antibody MG, particularly for early-onset cases of MG (e.g., patients younger than 50 years). Hyperplastic thymus glands of patients with MG contain T cells, B cells, plasma cells, and muscle-like (“myoid”) cells that express AChR. It is generally believed that the autoimmune response begins in the thymus and is subsequently exported to the periphery, where damage to the postsynaptic muscle end plate occurs, as described above. In early-onset MG, most patients have hyperplastic thymus glands (i.e., lymphofollicular thymic hyperplasia). In late-onset MG, patients often do not have thymic abnormalities, and the role of the thymus in late-onset MG is less clear. Approximately 10% to 15% of generalized MG patients are found to have thymomas, which are found to have an abundance of autoreactive T cells. These autoreactive T cells are exported to the periphery and facilitate pathogenic B cells and their autoantibodies. MuSK-antibody MG patients tend to lack thymus pathology, and the role, if any, of the thymus in MuSK-antibody MG is unknown.

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