pubmed-article:17475881 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:17475881 | lifeskim:mentions | umls-concept:C0005758 | lld:lifeskim |
pubmed-article:17475881 | lifeskim:mentions | umls-concept:C0079293 | lld:lifeskim |
pubmed-article:17475881 | lifeskim:mentions | umls-concept:C0009528 | lld:lifeskim |
pubmed-article:17475881 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
pubmed-article:17475881 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
pubmed-article:17475881 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
pubmed-article:17475881 | lifeskim:mentions | umls-concept:C1511545 | lld:lifeskim |
pubmed-article:17475881 | lifeskim:mentions | umls-concept:C1517004 | lld:lifeskim |
pubmed-article:17475881 | lifeskim:mentions | umls-concept:C1523987 | lld:lifeskim |
pubmed-article:17475881 | pubmed:issue | 10 | lld:pubmed |
pubmed-article:17475881 | pubmed:dateCreated | 2007-5-3 | lld:pubmed |
pubmed-article:17475881 | pubmed:abstractText | Epidermolysis bullosa acquisita is a subepidermal blistering disease associated with tissue-bound and circulating autoantibodies against type VII collagen, a major constituent of the dermal-epidermal junction. The passive transfer of Abs against type VII collagen into mice induces a subepidermal blistering disease dependent upon activation of terminal complement components. To further dissect the role of the different complement activation pathways in this model, we injected C1q-deficient, mannan-binding lectin-deficient, and factor B-deficient mice with rabbit Abs against murine type VII collagen. The development and evolution of blistering had a similar pattern in mannan-binding lectin-deficient and control mice and was initially only marginally less extensive in C1q-deficient mice compared with controls. Importantly, factor B-deficient mice developed a delayed and significantly less severe blistering disease compared with factor B-sufficient mice. A significantly lower neutrophilic infiltration was observed in factor B-deficient mice compared with controls and local reconstitution with granulocytes restored the blistering disease in factor B-deficient mice. Our study provides the first direct evidence for the involvement of the alternative pathway in an autoantibody-induced blistering disease and should facilitate the development of new therapeutic strategies for epidermolysis bullosa acquisita and related autoimmune diseases. | lld:pubmed |
pubmed-article:17475881 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17475881 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17475881 | pubmed:language | eng | lld:pubmed |
pubmed-article:17475881 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17475881 | pubmed:citationSubset | AIM | lld:pubmed |
pubmed-article:17475881 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17475881 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17475881 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17475881 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17475881 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17475881 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:17475881 | pubmed:month | May | lld:pubmed |
pubmed-article:17475881 | pubmed:issn | 0022-1767 | lld:pubmed |
pubmed-article:17475881 | pubmed:author | pubmed-author:ZillikensDetl... | lld:pubmed |
pubmed-article:17475881 | pubmed:author | pubmed-author:BottoMarinaM | lld:pubmed |
pubmed-article:17475881 | pubmed:author | pubmed-author:HolersV... | lld:pubmed |
pubmed-article:17475881 | pubmed:author | pubmed-author:TakahashiKazu... | lld:pubmed |
pubmed-article:17475881 | pubmed:author | pubmed-author:SitaruCassian... | lld:pubmed |
pubmed-article:17475881 | pubmed:author | pubmed-author:ThurmanJoshua... | lld:pubmed |
pubmed-article:17475881 | pubmed:author | pubmed-author:MihaiSidoniaS | lld:pubmed |
pubmed-article:17475881 | pubmed:author | pubmed-author:ChiriacMircea... | lld:pubmed |
pubmed-article:17475881 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:17475881 | pubmed:day | 15 | lld:pubmed |
pubmed-article:17475881 | pubmed:volume | 178 | lld:pubmed |
pubmed-article:17475881 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:17475881 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:17475881 | pubmed:pagination | 6514-21 | lld:pubmed |
pubmed-article:17475881 | pubmed:dateRevised | 2007-12-3 | lld:pubmed |
pubmed-article:17475881 | pubmed:meshHeading | pubmed-meshheading:17475881... | lld:pubmed |
pubmed-article:17475881 | pubmed:meshHeading | pubmed-meshheading:17475881... | lld:pubmed |
pubmed-article:17475881 | pubmed:meshHeading | pubmed-meshheading:17475881... | lld:pubmed |
pubmed-article:17475881 | pubmed:meshHeading | pubmed-meshheading:17475881... | lld:pubmed |
pubmed-article:17475881 | pubmed:meshHeading | pubmed-meshheading:17475881... | lld:pubmed |
pubmed-article:17475881 | pubmed:meshHeading | pubmed-meshheading:17475881... | lld:pubmed |
pubmed-article:17475881 | pubmed:meshHeading | pubmed-meshheading:17475881... | lld:pubmed |
pubmed-article:17475881 | pubmed:meshHeading | pubmed-meshheading:17475881... | lld:pubmed |
pubmed-article:17475881 | pubmed:meshHeading | pubmed-meshheading:17475881... | lld:pubmed |
pubmed-article:17475881 | pubmed:meshHeading | pubmed-meshheading:17475881... | lld:pubmed |
pubmed-article:17475881 | pubmed:meshHeading | pubmed-meshheading:17475881... | lld:pubmed |
pubmed-article:17475881 | pubmed:meshHeading | pubmed-meshheading:17475881... | lld:pubmed |
pubmed-article:17475881 | pubmed:meshHeading | pubmed-meshheading:17475881... | lld:pubmed |
pubmed-article:17475881 | pubmed:meshHeading | pubmed-meshheading:17475881... | lld:pubmed |
pubmed-article:17475881 | pubmed:year | 2007 | lld:pubmed |
pubmed-article:17475881 | pubmed:articleTitle | The alternative pathway of complement activation is critical for blister induction in experimental epidermolysis bullosa acquisita. | lld:pubmed |
pubmed-article:17475881 | pubmed:affiliation | Department of Dermatology, University of Lübeck, Lübeck, Germany, and Department of Pediatrics, Laboratory of Developmental Immunology, Massachusetts General Hospital, Boston 02115, USA. | lld:pubmed |
pubmed-article:17475881 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:17475881 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
pubmed-article:17475881 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
entrez-gene:12259 | entrezgene:pubmed | pubmed-article:17475881 | lld:entrezgene |
entrez-gene:14962 | entrezgene:pubmed | pubmed-article:17475881 | lld:entrezgene |
entrez-gene:17194 | entrezgene:pubmed | pubmed-article:17475881 | lld:entrezgene |
entrez-gene:17195 | entrezgene:pubmed | pubmed-article:17475881 | lld:entrezgene |
http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:17475881 | lld:pubmed |