Autoantibodies in myasthenia gravis target which molecule?

• A. Voltage-gated calcium channels
• B. Acetylcholine receptors
• C. Myelin basic protein
• D. Acetylcholinesterase

Answer: (B)

In myasthenia gravis the immune system makes antibodies against the postsynaptic nicotinic acetylcholine receptors at the neuromuscular junction. When these antibodies bind the receptors, they cause cross-linking and internalization of the receptors and activate complement, damaging the postsynaptic membrane and reducing the number of functional ACh receptors. With fewer receptors, the normally released acetylcholine fails to produce a sufficient end‑plate potential to trigger a muscle action potential, leading to fatigable weakness that worsens with use. That’s why therapies that boost acetylcholine in the synapse, like acetylcholinesterase inhibitors, can improve transmission. The other options point to different disorders or targets: antibodies against presynaptic voltage-gated calcium channels occur in Lambert-Eaton, myelin basic protein relates to demyelinating diseases like MS, and acetylcholinesterase is the enzyme that breaks down acetylcholine rather than a typical autoimmune target.