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dc.contributor.authorMartin, SF
dc.contributor.authorDudda, JC
dc.contributor.authorBachtanian, E
dc.contributor.authorLembo, A
dc.contributor.authorLiller, S
dc.contributor.authorDürr, C
dc.contributor.authorHeimesaat, MM
dc.contributor.authorBereswill, S
dc.contributor.authorFejer, Gyorgy
dc.contributor.authorVassileva, R
dc.contributor.authorJakob, T
dc.contributor.authorFreudenberg, N
dc.contributor.authorTermeer, CC
dc.contributor.authorJohner, C
dc.contributor.authorGalanos, C
dc.contributor.authorFreudenberg, MA
dc.date.accessioned2019-08-08T17:59:14Z
dc.date.available2019-08-08T17:59:14Z
dc.date.issued2008-09-01
dc.identifier.issn0022-1007
dc.identifier.issn1540-9538
dc.identifier.urihttp://hdl.handle.net/10026.1/14779
dc.description.abstract

<jats:p>Allergic contact hypersensitivity (CHS) is a T cell–mediated inflammatory skin disease. Interleukin (IL)-12 is considered to be important in the generation of the allergen-specific T cell response. Loss of IL-12 function in IL-12Rβ2–deficient mice, however, did not ameliorate the allergic immune response, suggesting alternate IL-12–independent pathways in the induction of CHS. Because exposure to contact allergens always takes place in the presence of microbial skin flora, we investigated the potential role of Toll-like receptors (TLRs) in the induction of CHS. Using mice deficient in TLR4, the receptor for bacterial lipopolysaccharide (LPS), IL-12 receptor (R) β2, or both, we show that the concomitant absence of TLR4 and IL-12Rβ2, but not the absence of TLR4 or IL-12Rβ2 alone, prevented DC-mediated sensitization, generation of effector T cells, and the subsequent CHS response to 2,4,6-trinitro-1-chlorobenzene (TNCB), oxazolone, and fluorescein isothiocyanate. Introduction of the TLR4 transgene into the TLR4/IL-12Rβ2 mutant restored the CHS inducibility, showing a requirement for TLR4 in IL-12–independent CHS induction. Furthermore, the concomitant absence of TLR2 and TLR4 prevented the induction of CHS to TNCB in IL-12–competent mice. Finally, CHS was inducible in germ-free wild-type and IL-12Rβ2–deficient mice, but not in germ-free TLR4/IL-12Rβ2 double deficient mice, suggesting that the necessary TLR activation may proceed via endogenous ligands.</jats:p>

dc.format.extent2151-2162
dc.format.mediumPrint-Electronic
dc.languageen
dc.language.isoeng
dc.publisherRockefeller University Press
dc.subjectAllergens
dc.subjectAnimals
dc.subjectCytokines
dc.subjectDermatitis, Contact
dc.subjectFemale
dc.subjectInterleukin-12
dc.subjectMale
dc.subjectMice
dc.subjectMice, Inbred BALB C
dc.subjectMice, Inbred C57BL
dc.subjectModels, Biological
dc.subjectSignal Transduction
dc.subjectToll-Like Receptor 2
dc.subjectToll-Like Receptor 4
dc.subjectToll-Like Receptors
dc.titleToll-like receptor and IL-12 signaling control susceptibility to contact hypersensitivity
dc.typejournal-article
dc.typeJournal Article
dc.typeResearch Support, Non-U.S. Gov't
plymouth.author-urlhttps://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000259656300019&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=11bb513d99f797142bcfeffcc58ea008
plymouth.issue9
plymouth.volume205
plymouth.publication-statusPublished
plymouth.journalThe Journal of Experimental Medicine
dc.identifier.doi10.1084/jem.20070509
plymouth.organisational-group/Plymouth
plymouth.organisational-group/Plymouth/Faculty of Health
plymouth.organisational-group/Plymouth/Faculty of Health/School of Biomedical Sciences
plymouth.organisational-group/Plymouth/REF 2021 Researchers by UoA
plymouth.organisational-group/Plymouth/REF 2021 Researchers by UoA/UoA01 Clinical Medicine
plymouth.organisational-group/Plymouth/Research Groups
plymouth.organisational-group/Plymouth/Research Groups/Institute of Translational and Stratified Medicine (ITSMED)
plymouth.organisational-group/Plymouth/Research Groups/Institute of Translational and Stratified Medicine (ITSMED)/CBR
plymouth.organisational-group/Plymouth/Users by role
plymouth.organisational-group/Plymouth/Users by role/Academics
plymouth.organisational-group/Plymouth/Users by role/Researchers in ResearchFish submission
dc.publisher.placeUnited States
dc.identifier.eissn1540-9538
dc.rights.embargoperiodNot known
rioxxterms.versionofrecord10.1084/jem.20070509
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserved
rioxxterms.typeJournal Article/Review


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