1 ds, cholera toxin B subunit and a monoclonal anti-GM1 antibody.

2 oth motor axonal AIP and selective serum IgG anti-GM1 antibodies.

3        Our results show that patient derived anti-GM1 antibodies and cholera toxin beta subunit impai

4 es was studied in transgenic mice exposed to anti-GM1 antibody and complement in ex vivo and in vivo

5                                              Anti-GM1 antibodies are present in some patients with au

6                          It is not clear how anti-GM1 antibodies cause nerve dysfunction and injury;

7   We asked whether passive transfer of human anti-GM1 antibodies from patients with GBS modulate axon

8               In contrast, low levels of IgG anti-GM1 antibodies (> 1:100) were detected in both the

9  the pathogenicity of immunoglobulin M (IgM) anti-GM1 antibodies in serum from patients with multifoc

10 e creation of rabbit models of anti-GD1b and anti-GM1 antibody-mediated sensory and motor neuropathy,

11 lia [GalNAcT-/--Tg(glial)], thereby allowing anti-GM1 antibodies to solely target GM1 in either axona

12                                        Human anti-GM1 antibodies were compared with other GM1 ligands

13                                              Anti-GM1 antibodies were found in 54% of C. jejuni-serop

14                                 In contrast, anti-GM1 antibodies were rare in sera that were either s

15 thies associated with elevated titers of IgM anti-GM1 antibodies, with increasing concentrations of i