| pubmed-article:9894851 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9894851 | lifeskim:mentions | umls-concept:C0038170 | lld:lifeskim |
| pubmed-article:9894851 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
| pubmed-article:9894851 | lifeskim:mentions | umls-concept:C1819433 | lld:lifeskim |
| pubmed-article:9894851 | lifeskim:mentions | umls-concept:C1553412 | lld:lifeskim |
| pubmed-article:9894851 | lifeskim:mentions | umls-concept:C1548328 | lld:lifeskim |
| pubmed-article:9894851 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:9894851 | pubmed:dateCreated | 1999-4-13 | lld:pubmed |
| pubmed-article:9894851 | pubmed:abstractText | Bacterial superantigens such as staphylococcal enterotoxin-A (SEA) have been implicated in the pathogenesis of psoriasis vulgaris. Major histocompatibility complex (MHC) class II molecules are high affinity receptors for SEA, and T cells found in psoriatic skin lesions express high levels of MHC class II. Here we address the question of whether SEA can directly activate psoriatic T cells in the absence of professional antigen-presenting cells. We show that SEA induces i) tyrosine phosphorylation of several proteins, ii) downregulation of the T-cell receptor (TCR), and iii) production of interferon-gamma (IFN-gamma), but not autocrine mitogenesis in CD8-positive T clones obtained from skin lesions of a patient with psoriasis vulgaris. Psoriatic T cells do not respond to SEA molecules if mutations are introduced in the TCRbeta- or in both the two MHC class II alpha- and beta-binding sites of SEA. Mutations in only one of the two MHC class II binding sites of SEA has different effects on T-cell activation. Thus, SEA molecules with a mutation in the MHC class II beta-binding site induce protein tyrosine phosphorylation, but not IFN-gamma production or co-stimulation of cytokine-mediated proliferation. In contrast, SEA with a mutation in the MHC class II alpha-binding site induces IFN-gamma and a qualitatively changed tyrosine phosphorylation profile. Both mutations delete the co-stimulatory effect on cytokine-mediated proliferation. This suggests that both MHC class II binding sites are involved in the autopresentation of SEA by psoriatic T cells. In conclusion, we provide evidence that SEA directly activates MVHC class H-positive psoriatic T-cell lines to produce IFN-gamma, a key cytokine in the pathogenesis of psoriasis vulgaris. | lld:pubmed |
| pubmed-article:9894851 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9894851 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9894851 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:9894851 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9894851 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9894851 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9894851 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9894851 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9894851 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9894851 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9894851 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:9894851 | pubmed:issn | 0001-2815 | lld:pubmed |
| pubmed-article:9894851 | pubmed:author | pubmed-author:BendtzenKK | lld:pubmed |
| pubmed-article:9894851 | pubmed:author | pubmed-author:RöpkeCC | lld:pubmed |
| pubmed-article:9894851 | pubmed:author | pubmed-author:SvejgaardAA | lld:pubmed |
| pubmed-article:9894851 | pubmed:author | pubmed-author:KaltoftKK | lld:pubmed |
| pubmed-article:9894851 | pubmed:author | pubmed-author:GeislerCC | lld:pubmed |
| pubmed-article:9894851 | pubmed:author | pubmed-author:OdumNN | lld:pubmed |
| pubmed-article:9894851 | pubmed:author | pubmed-author:DohlstenMM | lld:pubmed |
| pubmed-article:9894851 | pubmed:author | pubmed-author:NielsenM BMB | lld:pubmed |
| pubmed-article:9894851 | pubmed:author | pubmed-author:GerwienJJ | lld:pubmed |
| pubmed-article:9894851 | pubmed:author | pubmed-author:BregentholtSS | lld:pubmed |
| pubmed-article:9894851 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9894851 | pubmed:volume | 52 | lld:pubmed |
| pubmed-article:9894851 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9894851 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9894851 | pubmed:pagination | 530-8 | lld:pubmed |
| pubmed-article:9894851 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
| pubmed-article:9894851 | pubmed:meshHeading | pubmed-meshheading:9894851-... | lld:pubmed |
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| pubmed-article:9894851 | pubmed:meshHeading | pubmed-meshheading:9894851-... | lld:pubmed |
| pubmed-article:9894851 | pubmed:meshHeading | pubmed-meshheading:9894851-... | lld:pubmed |
| pubmed-article:9894851 | pubmed:meshHeading | pubmed-meshheading:9894851-... | lld:pubmed |
| pubmed-article:9894851 | pubmed:meshHeading | pubmed-meshheading:9894851-... | lld:pubmed |
| pubmed-article:9894851 | pubmed:meshHeading | pubmed-meshheading:9894851-... | lld:pubmed |
| pubmed-article:9894851 | pubmed:meshHeading | pubmed-meshheading:9894851-... | lld:pubmed |
| pubmed-article:9894851 | pubmed:meshHeading | pubmed-meshheading:9894851-... | lld:pubmed |
| pubmed-article:9894851 | pubmed:year | 1998 | lld:pubmed |
| pubmed-article:9894851 | pubmed:articleTitle | Staphylococcal enterotoxin-A directly stimulates signal transduction and interferon-gamma production in psoriatic T-cell lines. | lld:pubmed |
| pubmed-article:9894851 | pubmed:affiliation | Institute for Microbiology and Immunology, University of Copenhagen, Denmark. | lld:pubmed |
| pubmed-article:9894851 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9894851 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:9894851 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:9894851 | lld:pubmed |
