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dc.contributor.authorSigmundsdottir, Hen
dc.contributor.authorSigurgeirsson, Ben
dc.contributor.authorTroye-Blomberg, Men
dc.contributor.authorGood, M Fen
dc.contributor.authorValdimarsson, Hen
dc.contributor.authorJonsdottir, Ien
dc.date.accessioned2010-09-17T15:24:00Z
dc.date.available2010-09-17T15:24:00Z
dc.date.issued1997-06-01
dc.date.submitted2010-09-17
dc.identifier.citationScand. J. Immunol. 1997, 45(6):688-97en
dc.identifier.issn0300-9475
dc.identifier.pmid9201310
dc.identifier.urihttp://hdl.handle.net/2336/111298
dc.descriptionTo access publisher full text version of this article. Please click on the hyperlink in Additional Links fielden
dc.description.abstractPsoriasis is a T-cell mediated inflammatory skin disease which has been associated with group A, beta-haemolytic streptococcal infections. Four 20 a.a. long M6-peptides sharing 5-6 a.a. sequences with human epidermal keratins were identified. To investigate the role of potentially cross-reactive T cells in the pathogenesis of psoriasis, interferon-gamma (IFN-gamma) and interleukin-4 (IL-4) responses of circulating T cells to these peptides were analysed by ELISPOT and RT-PCR in 14 psoriatic patients, 12 healthy individuals and six patients with atopic dermatitis (AD). Untreated psoriatic patients' responses were significantly higher to these peptides than healthy and AD controls, while responses to a control M6-peptide, not sharing sequences with keratin, were negligible in all groups. No difference was found in response to streptokinase/streptodornase (SK/SD). M6-protein and peptides exclusively elicited IFN-gamma production, with little IL-4 production, even in AD patients. Interferon-gamma responses to all the M6-peptides were abolished after successful treatment of psoriatic patients, but responses to SK/SD were unaffected. The results indicate that active psoriasis is associated with Th1-like cells responding to streptococcal M6-peptides sharing sequences with human epidermal keratin. This is consistent with the hypothesis that psoriasis may be induced and exacerbated in susceptible individuals by M-protein specific Th1-like cells that cross-react with human epidermal keratin.
dc.language.isoenen
dc.publisherBlackwell Publishing Incen
dc.relation.urlhttp://www.ingentaconnect.com/content/bsc/sji/1997/00000045/00000006/art00289en
dc.subject.meshAdulten
dc.subject.meshAmino Acid Sequenceen
dc.subject.meshAntigens, Bacterialen
dc.subject.meshBacterial Outer Membrane Proteinsen
dc.subject.meshBacterial Proteinsen
dc.subject.meshCarrier Proteinsen
dc.subject.meshEpidermisen
dc.subject.meshFemaleen
dc.subject.meshGene Expression Regulationen
dc.subject.meshHumansen
dc.subject.meshInterferon-gammaen
dc.subject.meshInterleukin-4en
dc.subject.meshKeratinsen
dc.subject.meshLymphocyte Activationen
dc.subject.meshMaleen
dc.subject.meshMolecular Sequence Dataen
dc.subject.meshPsoriasisen
dc.subject.meshStreptococcus pyogenesen
dc.subject.meshStreptodornase and Streptokinaseen
dc.subject.meshT-Lymphocytesen
dc.titleCirculating T cells of patients with active psoriasis respond to streptococcal M-peptides sharing sequences with human epidermal keratinsen
dc.typeArticleen
dc.contributor.departmentDepartment of Immunology, National University Hospital, Reykjavik, Iceland.en
dc.identifier.journalScandinavian journal of immunologyen
html.description.abstractPsoriasis is a T-cell mediated inflammatory skin disease which has been associated with group A, beta-haemolytic streptococcal infections. Four 20 a.a. long M6-peptides sharing 5-6 a.a. sequences with human epidermal keratins were identified. To investigate the role of potentially cross-reactive T cells in the pathogenesis of psoriasis, interferon-gamma (IFN-gamma) and interleukin-4 (IL-4) responses of circulating T cells to these peptides were analysed by ELISPOT and RT-PCR in 14 psoriatic patients, 12 healthy individuals and six patients with atopic dermatitis (AD). Untreated psoriatic patients' responses were significantly higher to these peptides than healthy and AD controls, while responses to a control M6-peptide, not sharing sequences with keratin, were negligible in all groups. No difference was found in response to streptokinase/streptodornase (SK/SD). M6-protein and peptides exclusively elicited IFN-gamma production, with little IL-4 production, even in AD patients. Interferon-gamma responses to all the M6-peptides were abolished after successful treatment of psoriatic patients, but responses to SK/SD were unaffected. The results indicate that active psoriasis is associated with Th1-like cells responding to streptococcal M6-peptides sharing sequences with human epidermal keratin. This is consistent with the hypothesis that psoriasis may be induced and exacerbated in susceptible individuals by M-protein specific Th1-like cells that cross-react with human epidermal keratin.


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