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Quantification of Autoreactive Antibodies in Mice upon Experimental Autoimmune Encephalomyelitis
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Neuronal acetylcholine receptor autoimmunity.

Steven Vernino1

  • 1Department of Neurology, UT Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390-9036, USA. steven.vernino@utsouthwestern.edu

Annals of the New York Academy of Sciences
|June 24, 2008
PubMed
Summary
This summary is machine-generated.

Antibodies targeting ganglionic nicotinic acetylcholine receptors (AChRs) cause autoimmune autonomic ganglionopathy (AAG), a severe autonomic failure disorder. Immunomodulatory treatments show promise for AAG patients.

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Area of Science:

  • Neuroscience
  • Immunology

Background:

  • Nicotinic acetylcholine receptors (AChRs) are crucial ligand-gated cation channels in the nervous system.
  • Antibodies against muscle AChRs cause myasthenia gravis, while neuronal AChRs, though structurally similar, are pharmacologically distinct.
  • Ganglionic (alpha3-type) AChRs mediate fast synaptic transmission in autonomic ganglia.

Purpose of the Study:

  • To investigate the role of ganglionic AChR antibodies in autoimmune autonomic ganglionopathy (AAG).
  • To explore the potential for central nervous system AChRs to be targets of autoimmunity.

Main Methods:

  • Analysis of ganglionic AChR antibodies in AAG patients.
  • Induction of experimental AAG in rabbits via immunization or antibody transfer to mice.
  • Assessment of ganglionic AChR IgG effects on nicotinic membrane current in neuroblastoma cells.

Main Results:

  • Ganglionic AChR antibodies are present in up to 50% of AAG patients, who exhibit severe autonomic failure.
  • Experimental AAG models recapitulate human disease features.
  • Ganglionic AChR IgG inhibits nicotinic membrane current in cultured cells.
  • Antibodies against alpha7-type AChRs have been found in some encephalitis patients.

Conclusions:

  • AAG is an antibody-mediated neurological disorder similar to myasthenia gravis.
  • Plasma exchange and immunomodulatory treatments may improve AAG.
  • The role of central nervous system AChR antibodies in causing disease remains unclear.