Toll-like receptor and IL-12 signaling control susceptibility to contact hypersensitivity
dc.contributor.author | Martin, SF | |
dc.contributor.author | Dudda, JC | |
dc.contributor.author | Bachtanian, E | |
dc.contributor.author | Lembo, A | |
dc.contributor.author | Liller, S | |
dc.contributor.author | Dürr, C | |
dc.contributor.author | Heimesaat, MM | |
dc.contributor.author | Bereswill, S | |
dc.contributor.author | Fejer, Gyorgy | |
dc.contributor.author | Vassileva, R | |
dc.contributor.author | Jakob, T | |
dc.contributor.author | Freudenberg, N | |
dc.contributor.author | Termeer, CC | |
dc.contributor.author | Johner, C | |
dc.contributor.author | Galanos, C | |
dc.contributor.author | Freudenberg, MA | |
dc.date.accessioned | 2019-08-08T17:59:14Z | |
dc.date.available | 2019-08-08T17:59:14Z | |
dc.date.issued | 2008-09-01 | |
dc.identifier.issn | 0022-1007 | |
dc.identifier.issn | 1540-9538 | |
dc.identifier.uri | http://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.extent | 2151-2162 | |
dc.format.medium | Print-Electronic | |
dc.language | en | |
dc.language.iso | eng | |
dc.publisher | Rockefeller University Press | |
dc.subject | Allergens | |
dc.subject | Animals | |
dc.subject | Cytokines | |
dc.subject | Dermatitis, Contact | |
dc.subject | Female | |
dc.subject | Interleukin-12 | |
dc.subject | Male | |
dc.subject | Mice | |
dc.subject | Mice, Inbred BALB C | |
dc.subject | Mice, Inbred C57BL | |
dc.subject | Models, Biological | |
dc.subject | Signal Transduction | |
dc.subject | Toll-Like Receptor 2 | |
dc.subject | Toll-Like Receptor 4 | |
dc.subject | Toll-Like Receptors | |
dc.title | Toll-like receptor and IL-12 signaling control susceptibility to contact hypersensitivity | |
dc.type | journal-article | |
dc.type | Journal Article | |
dc.type | Research Support, Non-U.S. Gov't | |
plymouth.author-url | https://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000259656300019&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=11bb513d99f797142bcfeffcc58ea008 | |
plymouth.issue | 9 | |
plymouth.volume | 205 | |
plymouth.publication-status | Published | |
plymouth.journal | The Journal of Experimental Medicine | |
dc.identifier.doi | 10.1084/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.place | United States | |
dc.identifier.eissn | 1540-9538 | |
dc.rights.embargoperiod | Not known | |
rioxxterms.versionofrecord | 10.1084/jem.20070509 | |
rioxxterms.licenseref.uri | http://www.rioxx.net/licenses/all-rights-reserved | |
rioxxterms.type | Journal Article/Review |