Immunoelectron-microscopical labelling of glycolipids in the envelope of a demyelinating brain-derived RNA virus (Semliki Forest) by anti-glycolipid sera

Evans, N. R. S.; Webb, H. E.

doi:10.1016/0022-510x(86)90113-9

Cited by 12 publications

(3 citation statements)

References 24 publications

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“…Viral agents are hypothesized to lead to anti-ganglioside response via presentation of host ganglioside during viral budding from infected cells (Evans and Webb, 1986;Ang et al, 2000). The characteristics and pathological properties of our anti-GD1a antibodies and antisera arising in response to GD1a-KLH immunization were very similar to those seen in response to LOS immunization.…”

Section: Discussionsupporting

confidence: 51%

Overexpression of GD1a Ganglioside Sensitizes Motor Nerve Terminals to Anti-GD1a Antibody-Mediated Injury in a Model of Acute Motor Axonal Neuropathy

et al. 2005

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Anti-GD1a ganglioside antibodies (Abs) are the serological hallmark of the acute motor axonal form of the post-infectious paralysis, Guillain-Barré syndrome. Development of a disease model in mice has been impeded by the weak immunogenicity of gangliosides and the apparent resistance of GD1a-containing neural membranes to anti-GD1a antibody-mediated injury. Here we used mice with altered ganglioside biosynthesis to generate such a model at motor nerve terminals. First, we bypassed immunological tolerance by immunizing GD1a-deficient, ␤-1,4-N-acetylgalactosaminyl transferase knock-out mice with GD1a ganglioside-mimicking antigens from Campylobacter jejuni and generated high-titer anti-GD1a antisera and complement fixing monoclonal Abs (mAbs). Next, we exposed ex vivo nerve-muscle preparations from GD1a-overexpressing, GD3 synthase knock-out mice to the anti-GD1a mAbs in the presence of a source of complement and investigated morphological and electrophysiological damage. Dense antibody and complement deposits were observed only over presynaptic motor axons, accompanied by severe ultrastructural damage and electrophysiological blockade of motor nerve terminal function. Perisynaptic Schwann cells and postsynaptic membranes were unaffected. In contrast, normal mice were not only unresponsive to immunization with GD1a but also resistant to neural injury during anti-GD1a Ab exposure, demonstrating the central role of membrane antigen density in modulating both immune tolerance to GD1a and axonal susceptibility to anti-GD1a Abmediated injury. Identical paralyzing effects were observed when testing mouse and human anti-GD1a-positive sera. These data indicate that anti-GD1a Abs arise via molecular mimicry and are likely to be clinically relevant in injuring peripheral nerve axonal membranes containing sufficiently high levels of GD1a.

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Section: Discussionsupporting

confidence: 51%

Overexpression of GD1a Ganglioside Sensitizes Motor Nerve Terminals to Anti-GD1a Antibody-Mediated Injury in a Model of Acute Motor Axonal Neuropathy

et al. 2005

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“…The first possibility is that the CMV virion itself has a GM2-like epitope (e.g., a glycoprotein bearing a GM2-like structure or GM2 itself as part of the the virion membrane). 27 Furthermore, viral infection of fibroblasts may lead to an altered ganglioside pattern of cells. 28 Fetal brain cells infected with SV40 virus contained elevated levels of GM2.…”

Section: Figure 2 Specific Inhibition Of Anti-gm2 Reactivity By Cytomentioning

confidence: 99%

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

Ang¹,

Jacobs²,

Brandenburg³

et al. 2000

Neurology

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“…Semliki Forest virus is an enveloped virus and, as with any such virus, takes its envelope lipids from the membranes of the host cell. If virus is grown in mouse brain cell cultures, the envelope contains myelin glycolipids, including galactocerebroside Khalili-Shirazi et al, 1986;Evans and Webb, 1986).…”

Section: Semliki Forest Virusmentioning

confidence: 99%

Virus induced demyelination

Fazakerley¹,

Dyson²,

Simas³

1994

Journal of Neuroimmunology

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Immunoelectron-microscopical labelling of glycolipids in the envelope of a demyelinating brain-derived RNA virus (Semliki Forest) by anti-glycolipid sera

Cited by 12 publications

References 24 publications

Overexpression of GD1a Ganglioside Sensitizes Motor Nerve Terminals to Anti-GD1a Antibody-Mediated Injury in a Model of Acute Motor Axonal Neuropathy

Overexpression of GD1a Ganglioside Sensitizes Motor Nerve Terminals to Anti-GD1a Antibody-Mediated Injury in a Model of Acute Motor Axonal Neuropathy

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

Virus induced demyelination

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