TRANSPLACENTAL TRANSMISSION OF EXPERIMENTAL AUTOIMMUNE MYASTHENIA GRAVIS

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Abstract
Using neonates born from experimental autoimmune myasthenic rabbits, antibodies to acetylcholine receptor (AChR) were demonstrated in the newborn sera. By radioimmunoassay, antibody titers of 1-day-old neonates were roughly 1/7-1/9 of the mothers. At 8 wk postpartum, the antibody was no longer detectable. Ultrastructural observations of the intercostal muscles of the neonates revealed 2 types of changes. The 1st type was degenerative alterations in the postsynaptic membrane. The 2nd type of change, which was morphometrically analyzed, was immaturity of postsynaptic membrane structure with underdeveloped secondary synaptic clefts. After 28 days postpartum, these changes were not visible, indicating that the process is reversible as the antibody titer decreases. Apparenlty, the antibody to AChR, transferred transplacentally, arrested the development of postsynaptic structure, although reversibly, by blocking of the receptor sites in the end-plate.