Recent Advances in Structural Basis for Molecular Mimicry in Inflammatory Autoimmune Demyelinating Polyneuropathy - Molecules: Nucleation, Aggregation and Crystallization - page 310

(Koga et al ., 2001) and showed that the production of anti-GT1a/
anti-GQ1b auto-antibodies are mediated by the GT1a-mimicking and Gq1b-
mimicking lipooligosaccharides (LOSs) on this bacteria (Koga et al ., 2005a).
More importantly, Houliston et al . (2007) proved that the display by DH1
(a non-typical H. influenzae strain) of a surface glycan that mimics the termi-
nal trisaccharide portion of disialosyl-containing gangliosides provided strong
evidence for its involvement in the development of Fisher syndrome.
Other pathogens
In addition, Mycoplasma pneumoniae infection may be another candidate
for the pathogenesis of chronic polyneuropathy in GBS. Recently, Susuki
et al. (2004) demonstrated that, in certain cases, anti-GM1 antibodies
induced by molecular mimicry with M. pneumoniae may cause acute
motor axonal neuropathy.
The O-chains of a number of Helicobacter pylori strains exhibit
mimicry of Lewis x and Lewis y blood group antigens (Moran et al ., 1996).
By contrast, EBV and M. pneumoniae infection had no positive corre-
lation with MFS in a recent prospective case-control serologic study
(Koga et al ., 2005a). However, the details of these mimicries remain to
be investigated.
Molecular Pathogenesis
Oligosaccharides of LPSs that mimic
ganglioside structure
The presence of anti-GM1 antibody has been shown to be significantly
associated with preceding C. jejuni infection by numerous reports (Yu et al .,
2006), particularly with the Penner 19 strain (Table 1). Using gas-liquid
chromatography mass spectrometric (MS) analysis, Yuki and his col-
leagues firstly identified the purified LPSs of C. jejuni from a patient with
GBS who had anti-GM1 IgG antibody. MS and nuclear magnetic reso-
nance analyses have demonstrated many ganglioside-like structures in