Please use this identifier to cite or link to this item: https://doi.org/10.1586/1744666X.2013.811119
Title: Infectious and noninfectious triggers in Guillain-Barré syndrome
Authors: Wakerley, B.R.
Yuki, N. 
Keywords: acute inflammatory demyelinating polyneuropathy
acute motor axonal neuropathy
Bickerstaff brainstem encephalitis
Campylobacter jejuni
Fisher syndrome
Guillain-Barré syndrome
molecular mimicry
Issue Date: 2013
Citation: Wakerley, B.R., Yuki, N. (2013). Infectious and noninfectious triggers in Guillain-Barré syndrome. Expert Review of Clinical Immunology 9 (7) : 627-639. ScholarBank@NUS Repository. https://doi.org/10.1586/1744666X.2013.811119
Abstract: Guillain-Barré syndrome (GBS) is the commonest cause of acquired flaccid paralysis in the world and regarded by many as the prototype for postinfectious autoimmunity. Here the authors consider both infectious and noninfectious triggers of GBS and determine where possible what immunological mechanisms may account for this association. In approximately two-thirds of cases, an infectious trigger is reported in the weeks that lead up to disease onset, indicating that the host's response to infection must play an important role in disease pathogenesis. The most frequently identified bacteria, Campylobacter jejuni, through a process known as molecular mimicry, has been shown to induce cross-reactive anti-ganglioside antibodies, which can lead to the development of axonal-type GBS in some patients. Whether this paradigm can be extended to other infectious organisms or vaccines remains an important area of research and has public health implications. GBS has also been reported rarely in patients with underlying systemic diseases and immunocompromised states and although the exact mechanism is yet to be established, increased susceptibility to known infectious triggers should be considered most likely. © 2013 Informa UK Ltd.
Source Title: Expert Review of Clinical Immunology
URI: http://scholarbank.nus.edu.sg/handle/10635/126773
ISSN: 1744666X
DOI: 10.1586/1744666X.2013.811119
Appears in Collections:Staff Publications

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