Decrease in acetylcholine-receptor content of human myotube cultures mediated by monoclonal antibodies to α, β and γ subunits

AbstractOne of the two main causes of acetylcholine-receptor loss in myasthenia gravis is antigenic modulation, i.e. accelerated internalization and degradation rate by antibody-crosslinking. This phenomenon has been studied only in animal tissues. Therefore, we tested antigenic modulation of the acetylcholine receptor on human embryonic myotubes in culture. Several monoclonal antibodies to the α, β and γ subunits of the receptor reduced its concentration, in some cases down to one-third of the control. Some of these antibodies only form complexes of one antibody with two receptor molecules; consequently such small complexes are sufficient to accelerate internalization of the human acetylcholine receptor. This technique might be proved valuable for clinical screening of sera from myasthenie patients