Myasthenia gravis

https://doi.org/10.1016/0952-7915(93)90105-2Get rights and content

Abstract

The cause of the myasthenics' pathogenic autoantibody response against the muscle acetylcholine receptor is an intriguing puzzle involving the thymus and its epithelial tumours, and possibly a variety of cross-reacting epitopes. Another fascinating challenge is to find ways of selectively inhibiting this response in the patients.

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      In this heterogeneous disease it is possible to divide the patients into different subgroups depending on age of onset, clinical features, thymic histology, HLA associations [2,3], and the presence of either anti-AChR, or anti-MuSK antibodies [4]. The general consensus is that both genetic and environmental components play important roles in pathogenesis [5,6]. The known HLA associations with B8,A1, DR3 and DQ2 antigens in early-onset MG [7,8] differs in various populations, whereas Niks et al. [9] describe a strong association of MuSK antibody positive MG and HLA DR14-DQ5 in Caucasians.

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