Biology Reference
In-Depth Information
Another candidate for the pathogenesis of GBS might be CMV, which
has been proved to be correlated with anti-MAG/SGPG-positive chronic
polyneuropathy (Yuki et al ., 1998). However, until now there has been no
direct evidence to identify the carbohydrate structure of the SGPG epitope
in GBS-relative or MFS-relative CMV.
Chronic Inflammatory Demyelinating Polyneuropathy
Although GBS is clearly related to antecedent events, usually bacterial
or viral, no such clear association is evident in CIDP. Antibodies, par-
ticularly anti-ganglioside and cross reacting with epitopes on the pre-
cipitating infective organisms appear to play important roles in GBS
pathophysiology.
CIDP is characterized by progressive weakness and impaired sensory
function in the legs and arms that continue to progress for longer than
4 weeks. This disorder, which is sometimes called chronic relapsing
polyneuropathy, is caused by damage to the myelin sheath of the periph-
eral nerves (Toyka, Gold, 2003). Many monoclonal antibodies have been
found in patients with CIDP with high levels, including myelin-associated
glycoprotein (MAG) and SGPG (Yuki et al ., 1996).
Pathogenic auto-antibodies in CIDP
Unlike GBS, no glycolipid antigens have been identified as the targets of
auto-antibodies in CIDP pathogenesis (Willison, Yuki, 2002). So far,
many conflicting auto-antibodies have been found in patients with CIDP;
the reasons might come from the different detective methods being used
and the limited groups under study.
Among these antibodies have been sought to other myelin proteins,
including P2 and PMP22, in CIDP (Table 3), P0 is the only protein found
consistently. The potential importance of P0 as an auto-antigen is not sur-
prising because it constitutes 50% of peripheral nervous system (PNS)
myelin protein, and is illustrated by its ability to induce EAN (Zhu et al .,
2001).
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