@Article{ecn.2019.0424,
AUTHOR = {Zahra Ebrahim Soltani, Farzaneh Rahmani, Nima Rezaei},
TITLE = {Autoimmunity and cytokines in Guillain-Barré syndrome revisited: review of pathomechanisms with an eye on therapeutic options},
JOURNAL = {European Cytokine Network},
VOLUME = {30},
YEAR = {2019},
NUMBER = {1},
PAGES = {1--14},
URL = {http://www.techscience.com/ECN/v30n1/65397},
ISSN = {1952-4005},
ABSTRACT = {Guillain-Barré syndrome (GBS) is the most common cause of acute paralysis in the United States.
<i>Campylobacter jejuni</i> is a common trigger for GBS, igniting autoimmunity as a result of molecular mimicry between
<i>C. jejuni</i> 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. <i>C. jejuni</i> 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.},
DOI = {10.1684/ecn.2019.0424}
}