Literature DB >> 15102364

The Guillain-Barré syndrome: a true case of molecular mimicry.

C Wim Ang1, Bart C Jacobs, Jon D Laman.   

Abstract

Molecular mimicry between microbial antigens and host tissue forms an attractive hypothetical mechanism for the triggering of autoimmune disease by preceding infections. Recent crucial reviews state that molecular mimicry, as the causative mechanism, remains unproven for any human autoimmune disease. However, the peripheral neuropathy Guillain-Barré syndrome (GBS) is largely overseen in this debate. Based on recent evidence, we argue that GBS should be considered as an excellent paradigm and an attractive model for elucidation of both host and microbial aspects of molecular mimicry.

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Year:  2004        PMID: 15102364     DOI: 10.1016/j.it.2003.12.004

Source DB:  PubMed          Journal:  Trends Immunol        ISSN: 1471-4906            Impact factor:   16.687


  90 in total

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Review 7.  Pathophysiological actions of neuropathy-related anti-ganglioside antibodies at the neuromuscular junction.

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8.  Molecular mimicry: sensitization of Lewis rats with Campylobacter jejuni lipopolysaccharides induces formation of antibody toward GD3 ganglioside.

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9.  The crucial role of Campylobacter jejuni genes in anti-ganglioside antibody induction in Guillain-Barre syndrome.

Authors:  Peggy C R Godschalk; Astrid P Heikema; Michel Gilbert; Tomoko Komagamine; C Wim Ang; Jobine Glerum; Denis Brochu; Jianjun Li; Nobuhiro Yuki; Bart C Jacobs; Alex van Belkum; Hubert P Endtz
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