| pubmed-article:16234355 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16234355 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:16234355 | lifeskim:mentions | umls-concept:C0030805 | lld:lifeskim |
| pubmed-article:16234355 | lifeskim:mentions | umls-concept:C0064830 | lld:lifeskim |
| pubmed-article:16234355 | lifeskim:mentions | umls-concept:C0443146 | lld:lifeskim |
| pubmed-article:16234355 | lifeskim:mentions | umls-concept:C0443199 | lld:lifeskim |
| pubmed-article:16234355 | lifeskim:mentions | umls-concept:C1517004 | lld:lifeskim |
| pubmed-article:16234355 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:16234355 | pubmed:dateCreated | 2006-1-25 | lld:pubmed |
| pubmed-article:16234355 | pubmed:abstractText | Bullous pemphigoid (BP) is an autoimmune disease associated with autoantibodies directed against the hemidesmosomal antigens anti-BP230 and anti-B180. Neonatal mice injected with rabbit anti-mouse BP180 (mBP10) IgG develop a BP-like disease. Complement, immune complexes, mast cells, and neutrophils play a key role in subepidermal blistering in this animal model. In this study we investigated the role of beta2 integrins in experimental BP. Wild-type (WT) mice pretreated with neutralizing antibody against CD11a (LFA-1), CD11b (Mac-1), CD11a plus CD11b, or CD18 alone failed to develop BP when injected with pathogenic anti-mBP180 IgG. This was associated with a significant reduction in neutrophil accumulation in neutralizing antibody-treated mice. Mac-1-deficient (Mac-1 knockout [KO]) mice were resistant to experimental BP despite normal complement deposition and mast cell and neutrophil degranulation. Neutrophil infiltration in Mac-1 KO mice was severely impaired at 24 hours. However, more neutrophils accumulated in the skin of Mac-1 KO mice compared with WT mice at early time points (2-4 hours), which was associated with an increase in their survival as determined by apoptosis markers. These data suggest that beta2 integrins play differential roles in experimental BP: LFA-1 is required for neutrophil recruitment, while Mac-1 mediates late neutrophil accumulation and apoptosis of infiltrating neutrophils. | lld:pubmed |
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| pubmed-article:16234355 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16234355 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16234355 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:16234355 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:16234355 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16234355 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:16234355 | pubmed:issn | 0006-4971 | lld:pubmed |
| pubmed-article:16234355 | pubmed:author | pubmed-author:LiNingN | lld:pubmed |
| pubmed-article:16234355 | pubmed:author | pubmed-author:LiuZhiZ | lld:pubmed |
| pubmed-article:16234355 | pubmed:author | pubmed-author:DiazLuis ALA | lld:pubmed |
| pubmed-article:16234355 | pubmed:author | pubmed-author:MayadasTanya... | lld:pubmed |
| pubmed-article:16234355 | pubmed:author | pubmed-author:ZhaoMinglangM | lld:pubmed |
| pubmed-article:16234355 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16234355 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:16234355 | pubmed:volume | 107 | lld:pubmed |
| pubmed-article:16234355 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16234355 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16234355 | pubmed:pagination | 1063-9 | lld:pubmed |
| pubmed-article:16234355 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
| pubmed-article:16234355 | pubmed:meshHeading | pubmed-meshheading:16234355... | lld:pubmed |
| pubmed-article:16234355 | pubmed:meshHeading | pubmed-meshheading:16234355... | lld:pubmed |
| pubmed-article:16234355 | pubmed:meshHeading | pubmed-meshheading:16234355... | lld:pubmed |
| pubmed-article:16234355 | pubmed:meshHeading | pubmed-meshheading:16234355... | lld:pubmed |
| pubmed-article:16234355 | pubmed:meshHeading | pubmed-meshheading:16234355... | lld:pubmed |
