Por favor, use este identificador para citar o enlazar a este item:
http://hdl.handle.net/10261/15721
COMPARTIR / EXPORTAR:
SHARE CORE BASE | |
Visualizar otros formatos: MARC | Dublin Core | RDF | ORE | MODS | METS | DIDL | DATACITE | |
Campo DC | Valor | Lengua/Idioma |
---|---|---|
dc.contributor.author | Gallardo, Soledad | - |
dc.contributor.author | Córdoba, Blanca | - |
dc.contributor.author | Posada de la Paz, Manuel | - |
dc.contributor.author | Pozo, Victoria del | - |
dc.contributor.author | Messeguer Peypoch, Ángel | - |
dc.contributor.author | David, Chella S. | - |
dc.contributor.author | Lahoz, Carlos | - |
dc.date.accessioned | 2009-08-05T12:31:58Z | - |
dc.date.available | 2009-08-05T12:31:58Z | - |
dc.date.issued | 2005-06-24 | - |
dc.identifier.citation | Toxicology Letters 159(2): 173-181 (2005) | en_US |
dc.identifier.issn | 0378-4274 | - |
dc.identifier.uri | http://hdl.handle.net/10261/15721 | - |
dc.description | 9 pages, 3 figures.-- PMID: 15979827 [PubMed].-- Printed version published Nov 15, 2005. | en_US |
dc.description.abstract | Toxic oil syndrome (TOS) was described in Spain in 1981, due to the ingestion of contaminated rapeseed oil denatured with 2% aniline. More than 20,000 persons were affected, causing over 2500 deaths. Immunological findings were: eosinophilia, mRNA for Th2 cytokines (IL-4 and IL-5) in lungs, elevated total IgE and sIL-2R and increase of DR2 HLA class II phenotypic frequency in patients died by TOS. Our objective is to test the genetic restriction found in humans using HLA transgenic mice. Results show that mice expressing human DR2 and DQ6 (both in linkage disequilibrium), had higher percentage of eosinophils (DQ6) and IgE (DR2) than other transgenic mice tested (DR3 and DR4). Also, a Th2 shift was found in DR2 transgenic mice when toxic oil was administered with OVA. This has been corroborated by the IL-5 mRNA expression in 4 out of 6 lung tissues from TOS oil treated BALB/c mice. | en_US |
dc.description.abstract | These data indicate that an immunological response was induced as consequence of the toxic administration. These results correlate with those found in TOS patients and reinforce the implication of genetic restrictions in the acquisition of toxic-mediated disease. | en_US |
dc.description.sponsorship | This work has been supported by Red Española para Investigacion Enfermedades Raras (REpIER), G03/123 and Instituto Investigación de Enfermedades Raras de Base Genética (INERGEN). The HLA class II-transgenic mice used in this study were produced with support from NIH Grant AI-14764. | en_US |
dc.format.extent | 22195 bytes | - |
dc.format.mimetype | application/pdf | - |
dc.language.iso | eng | en_US |
dc.publisher | Elsevier | en_US |
dc.rights | closedAccess | en_US |
dc.subject | Toxic Oil Syndrome | en_US |
dc.subject | Toxiepidemic | en_US |
dc.subject | HLA | en_US |
dc.subject | Transgenic mice | en_US |
dc.subject | Eosinophilia | en_US |
dc.subject | Th2 pattern | en_US |
dc.title | Toxic oil syndrome: genetic restriction and immunomodulatory effects due to adulterated oils in a model of HLA transgenic mice | en_US |
dc.type | artículo | en_US |
dc.identifier.doi | 10.1016/j.toxlet.2005.05.009 | - |
dc.description.peerreviewed | Peer reviewed | en_US |
dc.relation.publisherversion | http://dx.doi.org/10.1016/j.toxlet.2005.05.009 | en_US |
dc.identifier.e-issn | 1879-3169 | - |
dc.type.coar | http://purl.org/coar/resource_type/c_6501 | es_ES |
item.openairetype | artículo | - |
item.grantfulltext | none | - |
item.cerifentitytype | Publications | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.fulltext | No Fulltext | - |
item.languageiso639-1 | en | - |
Aparece en las colecciones: | (IQAC) Artículos |
CORE Recommender
SCOPUSTM
Citations
8
checked on 29-mar-2024
WEB OF SCIENCETM
Citations
7
checked on 23-feb-2024
Page view(s)
329
checked on 22-abr-2024
Google ScholarTM
Check
Altmetric
Altmetric
NOTA: Los ítems de Digital.CSIC están protegidos por copyright, con todos los derechos reservados, a menos que se indique lo contrario.