Abstract
The experimental work discussed here endorses the hypothesis that in the pathogenesis of MG the initial and essential steps take place within the thymus. Most, if not all, thymuses of MG patients contain B cells capable of producing AChR-specific autoantibody along with appropriate stroma elements. This is especially pertinent in hyperplastic thymuses with germinal centers, which characteristically contain cellular complexes formed by AChR-producing MCs and surrounding interdigitating dendritic cells. The source of the myasthenogenic autoantigen is more complex in thymomas. There are data suggesting that thymoma epithelium express a protein that shares certain peptide epitopes with the AChR alpha chain, although there is no further molecular similarity. A unique type of "molecular self mimicry" could be the starter of thymoma-associated MG.
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