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oligosaccharides (OS) of bacteria isolated from patients with GBS and
MFS (Table 2).
GM1a, GD1a and GD3 mimics on
C. jejuni
strains were associated
with AMAN; GM2 was a possible target for IgM antibody in AIDP sub-
sequent to CMV infection; and anti-GQ1b antibody was found in patients
with MFS with antecedent infection (Koga
et al
., 2005a). Godschalk
et al
.
(2007) used high resolution magic angle spinning NMR spectroscopy to
realize the prediction of OS structures for the outer core structures of
26 GBS- and MFS-associated
C. jejuni
strains (Table 2).
Their data showed that molecular mimicry between gangliosides and
C. jejuni
LPSs is the presumable pathogenic mechanism in most cases of
C. jejuni
-related GBS. However, in some cases, other mechanisms may
play a role.
Since the GM1 epitope has been found on the LPSs of
H. influenzae
iso-
lated from a patient with AMAN (Mori
et al
., 2001), the GQ1b epitope is
another attracting mimic LPS structure on
H. influenzae
in patients with MFS
(Table 1). Moreover, LPSs of
Bruchella melitensis
(
B. melitensis
) were
reported to have a GM1 ganglioside-like structure by Watanabe
et al
. (2005).
Oligosaccharides of LPSs or other molecules
that mimic non-ganglioside structures
Potential pathogenic roles exist for other known and unknown glycol-
ipids enriched in the Schwann cell, myelin, and axonal membranes, such
as sulfated glucuronyl paragloboside (SGPG) (Yuki
et al
., 1996), galacto-
cerebroside, LM1, and sulfatides (Yu
et al
., 2006). These nonganglioside-
like structures also have microbial glycan mimics and could be important
in the pathogenesis of neuropathy in some patients with GBS.
Galactocerebroside (GalCer) epitope, a major glycolipid in nerv-
ous tissue, is present in
M. pneumoniae
, the infection that precedes
5% or 6% of GBS cases (Jacobs
et al
., 1998). At present, the carbo-
hydrate structures in
M. pneumoniae
are not clearly understood,
but there is a possible involvement of a GalCer-like epitope (Susuki
et al
., 2004).
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