Previously, we reported that
IgA anti-GM1 antibody is more closely associated with preceding Campylobacter jejuni
enteritis in
Guillain-Barré syndrome (GBS) than are
IgG and
IgM antibodies. However, the mechanism of the induction of
IgA anti-
ganglioside antibodies is not clear. In this study, serum
IgA antibodies against GM1,
GM1b, and GD1a, and
GalNAc-GD1a were examined in 152 GBS patients. In GBS, antecedent C. jejuni
infection is closely associated with
IgA antibodies, other than GM1, against
GM1b. The
IgA subclass distribution is completely restricted to
IgA1, no
secretory IgA anti-
ganglioside antibody being detected. This result does not support the hypothesis that the serum
IgA antibodies present in GBS after C. jejuni
enteritis originate at mucosal sites, such as the gut mucosal immune system. Seventeen (85%) of 20 patients with
IgA anti-
ganglioside antibodies had serological evidence of C. jejuni
infection and/or a history of antecedent
diarrhea. Moreover, a motor nerve conduction study showed that patients with
IgA antibodies frequently had axonal neuropathy, whereas none had demyelinating neuropathy. This may support the previous report that
IgA isotype anti-GM1
antibodies are more closely associated with poor outcome than are the
IgG or
IgM isotypes. The induction mechanism of
IgA anti-
ganglioside antibodies must be clarified by determining whether concentrations of
cytokines, which increase the
IgA class switch, are elevated in patients with GBS after C. jejuni
enteritis.