• Campylobacter jejuni
• Guillain-Barré syndrome

• PBMCs, peripheral blood mononuclear cells

Evidence is accumulating that anti-ganglioside antibodies may well mediate both Miller Fisher syndrome and the acute motor axonal form of Guillain-Barré syndrome ¹ but such antibodies are not present in most patients with the more common demyelinating forms of Guillain-Barré syndrome. T cells are thought to play an important part in the pathogenesis of the neuropathy in these patients, by analogy with experimental allergic neuritis and from histological studies of biopsy and postmortem peripheral nerve material. Furthermore many anti-ganglioside antibodies are of the IgG isotype normally requiring T cell help in their production.

We have previously proposed that γδ T cells might have a role in the pathogenesis of inflammatory demyelinating neuropathy after Campylobacter jejuni infection of the gut, because of their potential to react with carbohydrate ligands.² It is possible to culture γδ T cell lines from peripheral …