Anti-GD1a antibody is associated with axonal but not demyelinating forms of Guillain-Barr� syndrome

Abstract

Immunopathological studies suggest that the target of immune attack is different in the subtypes of Guillain‐Barré syndrome (GBS). In acute motor axonal neuropathy (AMAN), the attack appears directed against the axolemma and nodes of Ranvier. In acute inflammatory demyelinating polyneuropathy (AIDP), the attack appears directed against a component of the Schwann cell. However, the nature of the antigenic targets is still not clear. We prospectively studied 138 Chinese GBS patients and found that IgG anti‐GD1a antibodies were closely associated with AMAN but not AIDP. With a cutoff titer of greater than 1:100, 60% of AMAN versus 4% of AIDP patients had IgG anti‐GD1a antibodies; with a cutoff titer of greater than 1:1,000, 24% of AMAN patients and none of the AIDP patients had IgG anti‐GD1a antibodies. In contrast, low levels of IgG anti‐GM1 antibodies (>1:100) were detected in both the AMAN and the AIDP forms (57% vs 35%, NS). High titers of IgG anti‐GM1 (>1:1,000) were more common in the AMAN form (24% vs 8%, NS). Serological evidence of recent Campylobacter infection was detected in 81% of AMAN and 50% of AIDP patients, and anti‐ganglioside antibodies were common in both Campylobacter‐infected and noninfected patients. Our results suggest that IgG anti‐GD1a antibodies may be involved in the pathogenesis of AMAN. Ann Neurol 1999;45:168–173

Increased circulating T cell reactivity to GM3 and GQ1b gangliosides in primary progressive multiple sclerosis

“…30 Anti-GQ1b antibodies are elevated in patients with the Miller Fisher syndrome of ophthalmoplegia, ataxia and areflexia, 31 and increased anti-GD1a antibodies are associated with the acute motor axonal neuropathy subtype of the Guillain-Barre syndrome. 32 Furthermore, the induction of experimental sensory ataxic neuropathy in rabbits by immunization with GD1b3 proves that antiganglioside responses can be pathogenic.…”

Guillain–Barré syndrome: a century of progress

“…In 1990, Yuki postulated that anti-ganglioside antibodies might be present in a patient with AMAN following C.jejuni enteritis; he identified high titres of anti-GM1 IgG, which fell with resolution of the illness 41 .Numerous subsequent studies established that anti-GM1 IgG are present in a high proportion of patients with GBS, mostly those with AMAN or AMSAN 55 . Other anti-ganglioside antibodies were subsequently associated with specific clinical subtypes of GBS, including anti-GD1a antibodies with AMAN 56 and anti-GQ1b and anti-GT1a with acute oropharyngeal palsy 57 .…”

Guillain-Barré Syndrome

“…However, antibodies to GM1 or GD1b are not necessary poor prognostic markers, since three GBS patients with poor recovery and inability to walk at 1 year had no such antibodies but had serological evidence of recent C. jejuni infection [43]. IgG antibodies to GD1a are highly associated with AMAN, being detectable in 60 % of AMAN cases and only 4 % of AIDP [31]. While we do not recommend routine antibody testing in GBS, MFS is a notable exception [44,45].…”

“…Another proposed explanation is that axonal degeneration may involve the most distal nerve terminals. Molecular mimicry is suggested as the pathogenetic mechanism of AMAN based on the strong association with C. jejuni infection [31]. The lipopolysaccharide capsule of the C. jejuni shares epitopes with GM1 and GD1a resulting in cross-reacting antibodies.…”