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dc.contributor.authorSigmundsdottir, Hekla
dc.contributor.authorJohnston, Andrew
dc.contributor.authorGudjonsson, Johann Eli
dc.contributor.authorValdimarsson, Helgi
dc.date.accessioned2007-11-05T16:00:12Z
dc.date.available2007-11-05T16:00:12Z
dc.date.issued2004-04-01
dc.date.submitted2007-11-05
dc.identifier.citationClin. Immunol. 2004, 111(1):119-25en
dc.identifier.issn1521-6616
dc.identifier.pmid15093560
dc.identifier.doi10.1016/j.clim.2004.01.003
dc.identifier.urihttp://hdl.handle.net/2336/14484
dc.descriptionTo access publisher full text version of this article. Please click on the hyperlink in Additional Links fielden
dc.description.abstractAt both cutaneous and mucosal sites, interleukin (IL)-10, IL-12 and transforming growth factor (TGF)-beta are important regulators of chronic inflammatory disease, where cutaneous lymphocyte-associated antigen (CLA) and alphaE integrin (CD103) may be expressed. Stimulation with streptococcal pyrogenic exotoxin C (SpeC) increased the expression of CD103 by CD8+ but not CD4+ T cells. While adding IL-12 augmented the expression of CLA, superantigen-induced expression of CD103 was markedly suppressed by IL-12, which could be reversed by TGF-beta. Antibodies against TGF-beta inhibited, and a combination of anti-TGF-beta and IL-12 completely abrogated the induced CD103 expression. IL-10 strongly decreased the frequency of CLA+ and although not increasing the frequency of CD103+CD8+ T cells, the amount of CD103 expressed per cell was markedly increased. Thus, the expression of CLA and CD103 may be antagonistically regulated by IL-10 and IL-12 and the balance between these cytokines could influence the T cell migration of inflammatory cells into epithelial tissues.
dc.language.isoenen
dc.publisherAcademic Pressen
dc.relation.urlhttp://www.sciencedirect.com/science/article/B6WCJ-4BYJWNR-3/2/6d3ba165a5ce5b3c5a687d94c27bfdb6en
dc.subject.meshAntigens, CDen
dc.subject.meshCD8-Positive T-Lymphocytesen
dc.subject.meshIntegrin alpha Chainsen
dc.subject.meshInterleukin-12en
dc.subject.meshMembrane Glycoproteinsen
dc.subject.meshSuperantigensen
dc.subject.meshCD8-Positive T-Lymphocytesen
dc.titleDifferential effects of interleukin 12 and interleukin 10 on superantigen-induced expression of cutaneous lymphocyte-associated antigen (CLA) and alphaEbeta7 integrin (CD103) by CD8+ T cellsen
dc.typeArticleen
dc.identifier.journalClinical immunology (Orlando, Fla.)en
dc.format.digYES
html.description.abstractAt both cutaneous and mucosal sites, interleukin (IL)-10, IL-12 and transforming growth factor (TGF)-beta are important regulators of chronic inflammatory disease, where cutaneous lymphocyte-associated antigen (CLA) and alphaE integrin (CD103) may be expressed. Stimulation with streptococcal pyrogenic exotoxin C (SpeC) increased the expression of CD103 by CD8+ but not CD4+ T cells. While adding IL-12 augmented the expression of CLA, superantigen-induced expression of CD103 was markedly suppressed by IL-12, which could be reversed by TGF-beta. Antibodies against TGF-beta inhibited, and a combination of anti-TGF-beta and IL-12 completely abrogated the induced CD103 expression. IL-10 strongly decreased the frequency of CLA+ and although not increasing the frequency of CD103+CD8+ T cells, the amount of CD103 expressed per cell was markedly increased. Thus, the expression of CLA and CD103 may be antagonistically regulated by IL-10 and IL-12 and the balance between these cytokines could influence the T cell migration of inflammatory cells into epithelial tissues.


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