T cell recognition of a non-protein antigen preparation of Campylobacter jejuni in patients with Guillain-Barré syndrome
- J C Cooper1,
- S Hughes2,
- A Ben-Smith1,
- C O S Savage1,
- J B Winer2
- 1Birmingham Centre for Immune Regulation, Division of Medical Sciences, The Medical School, University of Birmingham, Edgbaston, Birmingham, UK
- 2Department of Neurosciences, Queen Elizabeth Hospital, Edgbaston, Birmingham B15 2TH, UK
- Correspondence to: Dr J B Winer; j.b.winer{at}bham.ac.uk
- Received 3 August 2000
- Accepted 23 October 2001
- Revised 9 October 2001
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 …
