| pubmed-article:17603494 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17603494 | lifeskim:mentions | umls-concept:C0221920 | lld:lifeskim |
| pubmed-article:17603494 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
| pubmed-article:17603494 | lifeskim:mentions | umls-concept:C0033860 | lld:lifeskim |
| pubmed-article:17603494 | lifeskim:mentions | umls-concept:C0254616 | lld:lifeskim |
| pubmed-article:17603494 | lifeskim:mentions | umls-concept:C1527148 | lld:lifeskim |
| pubmed-article:17603494 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:17603494 | pubmed:dateCreated | 2007-7-9 | lld:pubmed |
| pubmed-article:17603494 | pubmed:abstractText | Psoriasis is a common T cell-mediated autoimmune inflammatory disease. We show that blocking the interaction of alpha1beta1 integrin (VLA-1) with collagen prevented accumulation of epidermal T cells and immunopathology of psoriasis. Alpha1beta1 integrin, a major collagen-binding surface receptor, was exclusively expressed by epidermal but not dermal T cells. Alpha1beta1-positive T cells showed characteristic surface markers of effector memory cells and contained high levels of interferon-gamma but not interleukin-4. Blockade of alpha1beta1 inhibited migration of T cells into the epidermis in a clinically relevant xenotransplantation model. This was paralleled by a complete inhibition of psoriasis development, comparable to that caused by tumor necrosis factor-alpha blockers. These results define a crucial role for alpha1beta1 in controlling the accumulation of epidermal type 1 polarized effector memory T cells in a common human immunopathology and provide the basis for new strategies in psoriasis treatment focusing on T cell-extracellular matrix interactions. | lld:pubmed |
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| pubmed-article:17603494 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17603494 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17603494 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:17603494 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17603494 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:17603494 | pubmed:issn | 1078-8956 | lld:pubmed |
| pubmed-article:17603494 | pubmed:author | pubmed-author:GardnerHumphr... | lld:pubmed |
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| pubmed-article:17603494 | pubmed:author | pubmed-author:ConradCurdinC | lld:pubmed |
| pubmed-article:17603494 | pubmed:author | pubmed-author:BoymanOnurO | lld:pubmed |
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| pubmed-article:17603494 | pubmed:author | pubmed-author:KotelianskiVi... | lld:pubmed |
| pubmed-article:17603494 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17603494 | pubmed:volume | 13 | lld:pubmed |
| pubmed-article:17603494 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17603494 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17603494 | pubmed:pagination | 836-42 | lld:pubmed |
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| pubmed-article:17603494 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:17603494 | pubmed:articleTitle | Alpha1beta1 integrin is crucial for accumulation of epidermal T cells and the development of psoriasis. | lld:pubmed |
| pubmed-article:17603494 | pubmed:affiliation | Department of Dermatology, University Hospital of Zurich, Gloriastrasse 31, 8091 Zurich, Switzerland. curdin.conrad@usz.ch | lld:pubmed |
| pubmed-article:17603494 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17603494 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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