Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Myasthenia Gravis ll: Pathophysiology01:22

Myasthenia Gravis ll: Pathophysiology

The disease process of myasthenia gravis begins at the neuromuscular junction, where antibodies attack key proteins needed for muscle activation. This immune reaction weakens signal transmission, leading to the characteristic muscle fatigue and weakness that define the condition.Immune-Mediated DamageIn most individuals, antibodies target acetylcholine receptors (AChRs) on the postsynaptic membrane of muscle cells. By blocking acetylcholine binding, these antibodies prevent the nerve signal...
Myasthenia Gravis: Overview and Treatment01:20

Myasthenia Gravis: Overview and Treatment

Myasthenia gravis is a neuromuscular transmission disorder characterized by weakness and increased fatigability of skeletal muscles. It is an autoimmune disease affecting approximately one in 2000 people, where antibodies against the α1 subunit of nicotinic acetylcholine receptors are produced.
These antibodies interfere with the function of the nicotinic receptors in three ways: by binding to the receptor and disrupting acetylcholine binding; by causing cross-linking of receptors which leads...
Myasthenia Gravis: Diagnostic Tests01:15

Myasthenia Gravis: Diagnostic Tests

Myasthenia gravis is an autoimmune condition affecting neuromuscular transmission, causing generalized weakness in skeletal muscles. Initial diagnoses rely on patients' signs, symptoms, and medical history. The challenge lies in distinguishing myasthenia from other muscular dystrophies. An important diagnostic feature is the significant improvement of symptoms after administering anticholinesterase inhibitors.
The edrophonium test is a diagnostic tool for myasthenia gravis. It involves...
Chemical Synapses01:26

Chemical Synapses

Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...
Chemical Synapses01:26

Chemical Synapses

Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...
Complement System01:27

Complement System

The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a membrane...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Effect of immunotherapy on seizure severity and spike-wave index in epileptic encephalopathy with spike-wave activation in sleep: The value of EEG spikes in monitoring treatment response.

Epilepsy research·2026
Same author

Impact of Intravenous Immunoglobulin on Neuroinflammation Markers in Patients With Electrical Status Epilepticus During Slow Sleep.

In vivo (Athens, Greece)·2026
Same author

[Increased serum transferrin receptor 1 levels are associated with severity of acute ischemic stroke in patients with Covid-19 pneumonia].

Ideggyogyaszati szemle·2026
Same author

Immune-driven mechanisms in idiopathic intracranial hypertension: a critical synthesis.

Reviews in the neurosciences·2026
Same author

NLRP3 and RANK-RANKL-OPG Pathway-related Gene Expression Levels in Children With Autism Spectrum Disorder.

In vivo (Athens, Greece)·2026
Same author

Aquaporin-1 Antibodies in Autoimmune Inflammatory Demyelinating Disorders with Predominant Optic Nerve & Spinal Cord Involvement.

Noro psikiyatri arsivi·2026

Related Experiment Video

Updated: May 12, 2026

Antigenic Liposomes for Generation of Disease-specific Antibodies
10:31

Antigenic Liposomes for Generation of Disease-specific Antibodies

Published on: October 25, 2018

Complement associated pathogenic mechanisms in myasthenia gravis.

Erdem Tüzün1, Premkumar Christadoss

  • 1Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555-1070, USA.

Autoimmunity Reviews
|March 30, 2013
PubMed
Summary

The complement system

Area of Science:

  • Immunology
  • Neurology
  • Pathology

Background:

  • The complement system plays a critical role in the pathogenesis of myasthenia gravis (MG) and its animal model, experimental autoimmune myasthenia gravis (EAMG).
  • Accumulation of IgG and complement deposits at the neuromuscular junction (NMJ) is a hallmark of muscle pathology in both conditions.
  • This suggests that acetylcholine receptor antibodies (AChR-Ab) trigger muscle weakness via complement pathway activation and membrane attack complex (MAC) formation.

Purpose of the Study:

  • To investigate the role of the complement system in the pathogenesis of AChR-Ab related MG and EAMG.
  • To evaluate the therapeutic potential of complement inhibition strategies for MG treatment.

Main Methods:

  • Utilized complement factor C3 knockout (KO), C4 KO, and C5 deficient mice to assess EAMG resistance.

More Related Videos

Induction of Paralysis and Visual System Injury in Mice by T Cells Specific for Neuromyelitis Optica Autoantigen Aquaporin-4
09:29

Induction of Paralysis and Visual System Injury in Mice by T Cells Specific for Neuromyelitis Optica Autoantigen Aquaporin-4

Published on: August 21, 2017

Related Experiment Videos

Last Updated: May 12, 2026

Antigenic Liposomes for Generation of Disease-specific Antibodies
10:31

Antigenic Liposomes for Generation of Disease-specific Antibodies

Published on: October 25, 2018

Induction of Paralysis and Visual System Injury in Mice by T Cells Specific for Neuromyelitis Optica Autoantigen Aquaporin-4
09:29

Induction of Paralysis and Visual System Injury in Mice by T Cells Specific for Neuromyelitis Optica Autoantigen Aquaporin-4

Published on: August 21, 2017

  • Administered complement inhibitors including cobra venom factor, soluble complement receptor 1, anti-C1q, anti-C5, and anti-C6 antibodies to EAMG models.
  • Examined the susceptibility of decay accelerating factor (DAF) KO mice to EAMG.

    • Main Results:

    • Complement factor C3 KO, C4 KO, and C5 deficient mice demonstrated resistance to EAMG.
    • Treatment with various complement inhibitors ameliorated EAMG symptoms.
    • DAF KO mice exhibited increased susceptibility to EAMG, further implicating complement's role.

    Conclusions:

    • The complement system is fundamentally involved in AChR-Ab induced muscle weakness in MG and EAMG.
    • Inhibiting the classical and common complement pathways presents a promising therapeutic strategy for MG treatment.