What is Myasthenia Gravis?

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a) Diagram of a normal nerve cell releasing acetylcholine which binds to receptors on the muscle cell. This signal is processed and the muscle cell contracts. B) Diagram of myasthenia gravis. The nerve cell releases acetylcholine but anti-AChR antibodies bind to the acetylcholine so it cannot bind to the receptors on the muscle cells. Because the signal is blocked the muscle is paralyzed and does not contract.
Myasthenia gravis and impaired muscle contraction. (a) Normal release of the neurotransmitter acetylcholine stimulates muscle contraction. (b) In myasthenia gravis, autoantibodies block the receptors for acetylcholine (AChr) on muscle cells, resulting in paralysis.

Source: OpenStax Microbiology

OpenStax Microbiology

Autoantibodies directed against acetylcholine receptors (AChRs) in the synaptic cleft of neuromuscular junctions lead to myasthenia gravis. Anti-AChR antibodies are high-affinity IgGs and their synthesis requires activated CD4 T cells to interact with and stimulate B cells. Once produced, the anti-AChR antibodies affect neuromuscular transmission by at least three mechanisms:

  • Complement binding and activation at the neuromuscular junction
  • Accelerated AChR endocytosis of molecules cross-linked by antibodies
  • Functional AChR blocking, which prevents normal acetylcholine attachment to, and activation of, AChR

Regardless of the mechanism, the effect of anti-AChR is extreme muscle weakness and potentially death through respiratory arrest in severe cases.

Source:

Parker, N., Schneegurt, M., Thi Tu, A.-H., Forster, B. M., & Lister, P. (n.d.). Microbiology. Houston, Texas: OpenStax. Access for free at: https://openstax.org/details/books/microbiology

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