Anti-ganglioside antibodies
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| Autoantibody(s) | |
|---|---|
| Anti-ganglioside | |
| Common autoantibody characteristics | |
| Triggeringagent(s) | Campylobacter jejuni (Major)
Mycoplasma pneumoniae (Minor) Coeliac Disease(Rare) |
| Isoform specific | |
| autoantibody characteristics | |
| Autoantigen Isoform | Ganglidoside D3 (GD3) |
| Affected Organ(s) | Muscle |
| Affected Cells(s) | motor nerve terminal (nodes of Ranvier) |
| AssociatedDisease(s) | Guillain-Barré syndrome |
| Autoantibody class | IgA |
| Autoantigen Isoform | Ganglidoside M1 (GM1) |
| AssociatedDisease(s) | prodromal diarrhea |
| Autoantibody class | IgG |
| IgG Subclass | IgG1, IgG3, IgG4 |
| Autoantigen Isoform | Ganglidoside Q1b (GQ1b) |
| Affected Cells(s) | Schwann cells |
| AssociatedDisease(s) | Miller-Fisher Syndrome |
Anti-ganglioside antibodies react to self-gangliosides are found in autoimmune neuropathies. These antibodies were first found to react with cerebellar cells.[1] These antibodies show highest association with certain forms of Guillain-Barré syndrome.
Contents |
Antibodies to Ganglioside subtypes
Autoantigenic gangliosides that are currently known are GD3, GM1, GQ3 and GT1.
Anti-GD3
Anti-GD3 antibodies have been found in association with specific forms of Guillain-Barre syndrome. In vivo studies of isolated anti-GM1 and GD3 antibodies indicate the antibodies can interfere with motor neuron function.[1] Anti-GD1a antibodies were highly associated acute motor axonal neuropathy while high titers of anti-GM1 were more frequent indicating that GD1a possibly targets the axolemma and nodes of Ranvier[1] most of the Ab+ patients had C. jejuni infections. Patients with Anti-GalNAc-GD1a antibodies were less common but had more severe disease (rapidly progressive, predominantly distal weakness).[1]
Anti-GM1
Levels of anti-GM1 are elevated in patients with various forms of dementia.[1] Antibodies levels correlate with more severe Guillain-Barré syndrome.[1] In Japan, levels to GM1 were elevated in patients with prodromal diarrhea.[1] Titers to GM1 in other diseases (rheumatoid arthritis, primary Sjögren's syndrome and systemic lupus erythematosus) was also elevated.[1] additionally highly significant association was found with rheumatoid arthritis and peripheral neuropathies.[1] Conflicting evidence suggests no significant elevation in motor neuron neuropathy but marginally elevated IgA in sensory neuron neuropathies.[1] The autoimmune role of anti-GM1 is still unclear.
Anti-GQ1b
Anti-GQ1b are found in Miller-Fisher syndrome. Studies of these antibodies reveal large disruption of the Schwann cells. [1] Anti-GQ1b IgG levels were elevated in patients with ophthalmoplegia in Gullian-Barré syndrome[1]
Triggering agents
Microbial agents include: Campylobacter jejuni and Mycoplasma pneumoniae.[1]
Campylobacter jejuni
Antibodies to a GM1 epitope as well as to one with the GT1a or GD3 epitope were found in different strains of Campylobacter jejuni[1] and patients with Guillain-Barré syndrome have a high occurrence of C. jejuni infection[1]. Many studies indicate that C. jejuni may be causative for a subset of some forms of neuropathies.
Coeliac disease
Antibodies to ganglioside are found to be elevated in coeliac disease.[1] Recent studies show that gliadin can cross-linke to gangliosides in a transglutaminase indepedent manner, indicating that gliadin specific T-cell could present these antigens to the immune system.[1]
Immunoglobin isotypes
IgG. In multiple sclerosis, antibodies to GM1 are dominated by the IgG1, IgG3 and IgG4.[1] Also anti-GM1 IgG has been identified in Guillain-Barré syndrome or chronic inflammatory demyelinating polyradiculoneuropathy.[1] while controlled studies failed to find any significant association with these disease.[1] IgA. IgA to gangliosides have been observe in Gullien-Barre' syndrome. IgM. IgM antibodies have been detected in early work but their significance in disease is controversial.
