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NEUROLOGY 2003;61:994-996
© 2003 American Academy of Neurology
Brief Communications

{gamma}{delta} T cell non-responsiveness in Campylobacter jejuni–associated Guillain-Barré syndrome patients

I. Van Rhijn, PhD, T. Logtenberg, PhD, C. W. Ang, MD PhD and L. H. Van den Berg, MD PhD

From the Departments of Neurology (Drs. Van Rhijn and Van den Berg) and Immunology (Dr. Logtenberg), University Medical Center Utrecht; and the Departments of Neurology and Immunology (Dr. Ang), Erasmus University Rotterdam, the Netherlands.

Address correspondence and reprint requests to Dr. Leonard H. Van den Berg, Department of Neurology, Room G02.223, UMC Utrecht, P.O. Box 85500, 3508 GA Utrecht, the Netherlands; e-mail: l.h.vandenberg{at}neuro.azu.nl

To seek evidence for a role of molecular mimicry in the induction of Guillain-Barré syndrome (GBS), the authors studied Campylobacter jejuni–reactive T lymphocytes in patients with GBS. In contrast to controls, {gamma}{delta} T cells of patients with GBS with antecedent C jejuni infections failed to respond to C jejuni. Supplementing cell cultures with the cytokines interleukin-2 or interleukin-15 resulted in restoration of the {gamma}{delta} T cell proliferative response. {gamma}{delta} T cell non-responsiveness may lead to defective regulation of antibody production, and in this way an (auto)immune response against ganglioside-like epitopes on peripheral nerve may cause GBS.

Received July 22, 2002. Accepted in final form June 10, 2003.






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