Anti-GM1 Ganglioside Antibodies Cloned from Autoimmune Neuropathy Patients Show Diverse Binding Patterns in the Rodent Nervous System

O’Hanlon, Graham M.; Paterson, G; Wilson, G; Doyle, D; McHardie, P.; Willison, H J

doi:10.1097/00005072-199602000-00007

Cited by 45 publications

(18 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The immunocytochemical studies (which require affinity purified anti-GM1 Abs because normal human serum can have anti-neurofilament Abs and axonal binding (Stefansson et al, 1985)) with 98-7 Abs could not be performed because of limited quantity of this serum was available. Fine specificity experiments indicate that GM1 ligands used in this study have distinct reactivities to GM1-derivatives and this could be one factor that influences selective nerve fiber/target recognition, as was suggested previously (O'Hanlon et al, 1996;Lopez et al, 2008). Besides fine specificity of the Abs, accessibility of glycolipid antigens to Abs is also very important.…”

Section: Discussionsupporting

confidence: 76%

Passive Transfer of IgG Anti-GM1 Antibodies Impairs Peripheral Nerve Repair

López

Zhang

et al. 2010

Journal of Neuroscience

View full text Add to dashboard Cite

Anti-GM1 antibodies are present in some patients with autoimmune neurological disorders. These antibodies are most frequently associated with acute immune neuropathy called Guillain-Barré syndrome (GBS). Some clinical studies associate the presence of these antibodies with poor recovery in GBS. The patients with incomplete recovery have failure of nerve repair, particularly axon regeneration. Our previous work indicates that monoclonal antibodies can inhibit axon regeneration by engaging cell surface gangliosides (Lehmann et al., 2007). We asked whether passive transfer of human anti-GM1 antibodies from patients with GBS modulate axon regeneration in an animal model. Human anti-GM1 antibodies were compared with other GM1 ligands, cholera toxin B subunit and a monoclonal anti-GM1 antibody. Our results show that patient derived anti-GM1 antibodies and cholera toxin ␤ subunit impair axon regeneration/repair after PNS injury in mice. Comparative studies indicated that the antibody/ligand-mediated inhibition of axon regeneration is dependent on antibody/ligand characteristics such as affinity-avidity and fine specificity. These data indicate that circulating immune effectors such as human autoantibodies, which are exogenous to the nervous system, can modulate axon regeneration/nerve repair in autoimmune neurological disorders such as GBS.

show abstract

Section: Discussionsupporting

confidence: 76%

Passive Transfer of IgG Anti-GM1 Antibodies Impairs Peripheral Nerve Repair

López

Zhang

et al. 2010

Journal of Neuroscience

View full text Add to dashboard Cite

show abstract

“…[13][14][15] Antiganglioside antibodies can bind to peripheral nerves and may interfere with neuromuscular transmission. 16,17 These findings support the hypothesis that antiganglioside antibodies, induced by molecular mimicry, have a role in the development of GBS.…”

supporting

confidence: 78%

Cross-reactive antibodies against GM2 and CMV-infected fibroblasts in Guillain–Barré syndrome

Ang¹,

Jacobs²,

Brandenburg³

et al. 2000

Neurology

View full text Add to dashboard Cite

show abstract

“…2 These apparent differences may relate to (i) type (IgM vs. IgG), source and concentration of the anti-bodies tested; (ii) experimental design and method of application of the antibodies (to intact or desheathed nerve); and (iii) the high diversity and species differences of anti-GM1 antibodies in their peripheral nerve-staining pattern, including binding to nodes of Ranvier, as shown in immunohistological studies. 17 Pathophysiological Relevance. Under our conditions, high concentration of IgG anti-GM1 antibodies plus complement in surplus were required for a partial block of the Na + channels to occur.…”

Section: Discussionmentioning

confidence: 99%

Anti-GM1 antibodies can block neuronal voltage-gated sodium channels

et al. 2000

View full text Add to dashboard Cite

Anti‐GM1 antibodies, frequently found in the serum of patients with Guillain‐Barré syndrome (GBS), have been suggested to interfere with axonal function. We report that IgG anti‐GM1 antibodies, raised in rabbits, can reversibly block the voltage‐gated Na+ channels of nerve cells, thus causing a reduction of the excitatory Na+ current. The block was, however, only substantial when the antibodies were applied together with rabbit complement factors. A solution containing anti‐GM1 sera (dilution 1:100) and complement (1:50) reduced the Na+ current to 0.5 ± 0.2 times control (mean value ± SD). Applications of the antibody by itself, complement by itself, or anti‐GM2 or anti‐GM4 antibodies (1:100) plus complement had little effect. The complexes of anti‐GM1 antibodies and complement factors block the ion‐conducting pore of the channel directly. In addition, they increase the fraction of channels that are inactivated at the resting potential and alter channel function by changing the membrane surface charge. The described effects may be responsible for conduction slowing and reversible conduction failure in some GBS patients. © 2000 John Wiley & Sons, Inc. Muscle Nerve 23: 1414–1420, 2000.

show abstract

Anti-GM1 Ganglioside Antibodies Cloned from Autoimmune Neuropathy Patients Show Diverse Binding Patterns in the Rodent Nervous System

Cited by 45 publications

References 0 publications

Passive Transfer of IgG Anti-GM1 Antibodies Impairs Peripheral Nerve Repair

Passive Transfer of IgG Anti-GM1 Antibodies Impairs Peripheral Nerve Repair

Cross-reactive antibodies against GM2 and CMV-infected fibroblasts in Guillain–Barré syndrome

Anti-GM1 antibodies can block neuronal voltage-gated sodium channels

Contact Info

Product

Resources

About