ABSTRACT
The network theory as hypothesized by N. K. Jerne assumes the ability of anti-idiotype (anti-Id) antibodies both to suppress and to enhance specific immune responses. The receptor antibodies in the human disease are polyclonal. The antibodies differ with regard to binding sites on the receptor, isoelectric point, and reactivity with anti-Id antibodies. There is abundant evidence that all antibodies which bind to the acetylcholine receptor can disturb the neuromuscular function. Abnormal immune regulation has been suggested to contribute to the development and perpetuation of autoimmune disorders, and in human autoimmune diseases, autologous anti-Id have been demonstrated in myasthenia gravis, in systemic lupus erythematosus, in insulin-dependent diabetes, and in autoimmune disorders of the thyroid gland. There are two instances in which one can talk about a transient myasthenia gravis syndrome: one is neonatal myasthenia and the other is the penicillamine-induced disease.
