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Guillain–Barré syndrome, transverse myelitis and infectious diseases

dc.creatorRodríguez Velandia, Yhojan Alexisspa
dc.creatorRojas Quintana, Manuel Eduardospa
dc.creatorPacheco Nieva, Yovana
dc.creatorAcosta Ampudia, Yeny Yasbleidyspa
dc.creatorRamírez Santana, Heily Carolinaspa
dc.creatorMonsalve Carmona, Diana Marcela
dc.creatorGershwin, M Ericspa
dc.creatorAnaya, Juan-Manuelspa
dc.date.accessioned2020-05-26T00:03:57Z
dc.date.available2020-05-26T00:03:57Z
dc.date.created2018spa
dc.description.abstractGuillain–Barré syndrome (GBS) and transverse myelitis (TM) both represent immunologically mediated polyneuropathies of major clinical importance. Both are thought to have a genetic predisposition, but as of yet no specific genetic risk loci have been clearly defined. Both are considered autoimmune, but again the etiologies remain enigmatic. Both may be induced via molecular mimicry, particularly from infectious agents and vaccines, but clearly host factor and co-founding host responses will modulate disease susceptibility and natural history. GBS is an acute inflammatory immune-mediated polyradiculoneuropathy characterized by tingling, progressive weakness, autonomic dysfunction, and pain. Immune injury specifically takes place at the myelin sheath and related Schwann-cell components in acute inflammatory demyelinating polyneuropathy, whereas in acute motor axonal neuropathy membranes on the nerve axon (the axolemma) are the primary target for immune-related injury. Outbreaks of GBS have been reported, most frequently related to Campylobacter jejuni infection, however, other agents such as Zika Virus have been strongly associated. Patients with GBS related to infections frequently produce antibodies against human peripheral nerve gangliosides. In contrast, TM is an inflammatory disorder characterized by acute or subacute motor, sensory, and autonomic spinal cord dysfunction. There is interruption of ascending and descending neuroanatomical pathways on the transverse plane of the spinal cord similar to GBS. It has been suggested to be triggered by infectious agents and molecular mimicry. In this review, we will focus on the putative role of infectious agents as triggering factors of GBS and TM. © 2017, The Chinese Society of Immunology and The University of Science and Technology of China, All rights reserved.eng
dc.format.mimetypeapplication/pdf
dc.identifier.doihttps://doi.org/10.1038/cmi.2017.142
dc.identifier.issn16727681
dc.identifier.urihttps://repository.urosario.edu.co/handle/10336/23643
dc.language.isoengspa
dc.publisherChinese Soc Immunologyspa
dc.relation.citationEndPage562
dc.relation.citationIssueNo. 6
dc.relation.citationStartPage547
dc.relation.citationTitleCellular and Molecular Immunology
dc.relation.citationVolumeVol. 15
dc.relation.ispartofCellular and Molecular Immunology, ISSN:16727681, Vol.15, No.6 (2018); pp. 547-562spa
dc.relation.urihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85044178113&doi=10.1038%2fcmi.2017.142&partnerID=40&md5=a7766b37ceb5a0479ed605ea17c02579spa
dc.rights.accesRightsinfo:eu-repo/semantics/openAccess
dc.rights.accesoAbierto (Texto Completo)spa
dc.source.instnameinstname:Universidad del Rosariospa
dc.source.reponamereponame:Repositorio Institucional EdocURspa
dc.subject.keywordGangliosidespa
dc.subject.keywordtransverseeng
dc.subject.keywordHla antigenspa
dc.subject.keywordProtein antibodyspa
dc.subject.keywordAcute inflammatory demyelinating polyneuropathyspa
dc.subject.keywordAcute motor axonal neuropathyspa
dc.subject.keywordCampylobacter enteritisspa
dc.subject.keywordCellular immunityspa
dc.subject.keywordChikungunyaspa
dc.subject.keywordCytomegalovirus infectionspa
dc.subject.keywordDenguespa
dc.subject.keywordDisease associationspa
dc.subject.keywordGuillain barre syndromespa
dc.subject.keywordHaemophilus infectionspa
dc.subject.keywordHaemophilus influenzaespa
dc.subject.keywordHepatitis bspa
dc.subject.keywordHerpes simplexspa
dc.subject.keywordHerpes zosterspa
dc.subject.keywordHost resistancespa
dc.subject.keywordHumanspa
dc.subject.keywordHuman immunodeficiency virus infectionspa
dc.subject.keywordHumoral immunityspa
dc.subject.keywordInfectionspa
dc.subject.keywordInnate immunityspa
dc.subject.keywordMolecular mechanicsspa
dc.subject.keywordMycoplasma pneumoniaspa
dc.subject.keywordMyelitisspa
dc.subject.keywordNerve fiber membranespa
dc.subject.keywordNonhumanspa
dc.subject.keywordReviewspa
dc.subject.keywordZika feverspa
dc.subject.keywordCommunicable diseasespa
dc.subject.keywordGuillain barre syndromespa
dc.subject.keywordImmunityspa
dc.subject.keywordImmunologyspa
dc.subject.keywordMicrobiologyspa
dc.subject.keywordMyelitisspa
dc.subject.keywordPathologyspa
dc.subject.keywordVirologyspa
dc.subject.keywordCommunicable diseasesspa
dc.subject.keywordGuillain-barre syndromespa
dc.subject.keywordHumansspa
dc.subject.keywordImmunityspa
dc.subject.keywordMyelitiseng
dc.titleGuillain–Barré syndrome, transverse myelitis and infectious diseasesspa
dc.typearticleeng
dc.type.hasVersioninfo:eu-repo/semantics/publishedVersion
dc.type.spaArtículospa
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