Autoimmunity and cytokines in Guillain-Barré syndrome revisited: review of pathomechanisms with an eye on therapeutic options (notice n° 235798)

détails MARC
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control field 20250112063921.0
041 ## - LANGUAGE CODE
Language code of text/sound track or separate title fre
042 ## - AUTHENTICATION CODE
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100 10 - MAIN ENTRY--PERSONAL NAME
Personal name Ebrahim Soltani, Zahra
Relator term author
245 00 - TITLE STATEMENT
Title Autoimmunity and cytokines in Guillain-Barré syndrome revisited: review of pathomechanisms with an eye on therapeutic options
260 ## - PUBLICATION, DISTRIBUTION, ETC.
Date of publication, distribution, etc. 2019.<br/>
500 ## - GENERAL NOTE
General note 1
520 ## - SUMMARY, ETC.
Summary, etc. Guillain-Barré syndrome (GBS) is the most common cause of acute paralysis in the United States. Campylobacter jejuni is a common trigger for GBS, igniting autoimmunity as a result of molecular mimicry between C. jejuni lipooligosaccharide (LOS) and host gangliosides. Evidence also suggests an active role for cell-mediated and innate immunity in pathogenesis of GBS. Infection alone is not enough for GBS to develop, infection with the same strain might yield different outcomes in different patients. C. jejuni strains with low to absent molecular mimicry to self-antigens can cause full-blown GBS with positive autoantibodies. A role for T helper 17 and IL-17 in acute phase of GBS is also identified. Currently, no biological treatment is validated for severe, ventilation-dependent patients with GBS, who might not benefit from either IVIG or plasma exchange therapy. Use of biologic agents in treatment-resistant GBS, especially anti-IL-17 agents, such as secukinumab, ixekizumab, and brodalumab, is to be hoped. This review covers up-to-date knowledge on autoimmune mechanisms responsible in different subtypes of GBS: acute inflammatory demyelinating polyneuropathy and acute motor axonal neuropathy; as well as the experimental autoimmune neuritis (EAN), a commonly used animal model of GBS.
690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN)
Topical term or geographic name as entry element Guillain-Barré syndrome
690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN)
Topical term or geographic name as entry element Campylobacter jejuni
690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN)
Topical term or geographic name as entry element acute inflammatory demyelinating polyneuropathy
690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN)
Topical term or geographic name as entry element experimental autoimmune neuritis
690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN)
Topical term or geographic name as entry element acute motor axonal neuropathy
700 10 - ADDED ENTRY--PERSONAL NAME
Personal name Rahmani, Farzaneh
Relator term author
700 10 - ADDED ENTRY--PERSONAL NAME
Personal name Rezaei, Nima
Relator term author
786 0# - DATA SOURCE ENTRY
Note European Cytokine Network | Volume 30 | 1 | 2019-03-01 | p. 1-14 | 1148-5493
856 41 - ELECTRONIC LOCATION AND ACCESS
Uniform Resource Identifier <a href="https://shs.cairn.info/revue-european-cytokine-network-2019-1-page-1?lang=en">https://shs.cairn.info/revue-european-cytokine-network-2019-1-page-1?lang=en</a>

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