| pubmed-article:17726161 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17726161 | lifeskim:mentions | umls-concept:C0030705 | lld:lifeskim |
| pubmed-article:17726161 | lifeskim:mentions | umls-concept:C0330390 | lld:lifeskim |
| pubmed-article:17726161 | lifeskim:mentions | umls-concept:C0024501 | lld:lifeskim |
| pubmed-article:17726161 | lifeskim:mentions | umls-concept:C0017968 | lld:lifeskim |
| pubmed-article:17726161 | lifeskim:mentions | umls-concept:C0085278 | lld:lifeskim |
| pubmed-article:17726161 | lifeskim:mentions | umls-concept:C0235914 | lld:lifeskim |
| pubmed-article:17726161 | lifeskim:mentions | umls-concept:C0332157 | lld:lifeskim |
| pubmed-article:17726161 | lifeskim:mentions | umls-concept:C0205148 | lld:lifeskim |
| pubmed-article:17726161 | lifeskim:mentions | umls-concept:C0442802 | lld:lifeskim |
| pubmed-article:17726161 | lifeskim:mentions | umls-concept:C0721534 | lld:lifeskim |
| pubmed-article:17726161 | pubmed:issue | 13 | lld:pubmed |
| pubmed-article:17726161 | pubmed:dateCreated | 2007-12-6 | lld:pubmed |
| pubmed-article:17726161 | pubmed:abstractText | Antiphospholipid syndrome (APS) is an autoimmune prothrombotic disorder associated with autoantibodies to phospholipid (PL)-binding proteins, such as beta(2)-glycoprotein I (beta(2)GPI). We have recently reported that binding of beta(2)GPI to anionic PL facilitates processing and presentation of the cryptic beta(2)GPI epitope that activates pathogenic autoreactive T cells. To clarify mechanisms that induce sustained presentation of the dominant antigenic beta(2)GPI determinant in patients with APS, T-cell proliferation induced by beta(2)GPI-treated phosphatidylserine liposome (beta(2)GPI/PS) was evaluated in bulk peripheral blood mononuclear cell cultures. T cells from patients with APS responded to beta(2)GPI/PS in the presence of immunoglobulin G (IgG) anti-beta(2)GPI antibodies derived from APS plasma, and this response was completely inhibited either by the depletion of monocytes or by the addition of anti-FcgammaRI antibody. These findings indicate that efficient presentation of the cryptic determinants can be achieved by monocytes undergoing FcgammaRI-mediated uptake of beta(2)GPI-bound anionic surfaces in the presence of IgG anti-beta(2)GPI antibodies. Finally, beta(2)GPI-bound oxidized LDL or activated platelets also induced the specific T-cell response. Continuous exposure to these anionic surfaces may play a critical role in maintaining the pathogenic anti-beta(2)GPI antibody response in patients with APS. | lld:pubmed |
| pubmed-article:17726161 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17726161 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17726161 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:17726161 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17726161 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17726161 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17726161 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17726161 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17726161 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17726161 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17726161 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:17726161 | pubmed:issn | 0006-4971 | lld:pubmed |
| pubmed-article:17726161 | pubmed:author | pubmed-author:KaburakiJunic... | lld:pubmed |
| pubmed-article:17726161 | pubmed:author | pubmed-author:KuwanaMasatak... | lld:pubmed |
| pubmed-article:17726161 | pubmed:author | pubmed-author:KobayashiKazu... | lld:pubmed |
| pubmed-article:17726161 | pubmed:author | pubmed-author:MatsuuraEijiE | lld:pubmed |
| pubmed-article:17726161 | pubmed:author | pubmed-author:YamaguchiYuki... | lld:pubmed |
| pubmed-article:17726161 | pubmed:author | pubmed-author:SetaNoriyukiN | lld:pubmed |
| pubmed-article:17726161 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17726161 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:17726161 | pubmed:volume | 110 | lld:pubmed |
| pubmed-article:17726161 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17726161 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17726161 | pubmed:pagination | 4312-8 | lld:pubmed |
| pubmed-article:17726161 | pubmed:meshHeading | pubmed-meshheading:17726161... | lld:pubmed |
| pubmed-article:17726161 | pubmed:meshHeading | pubmed-meshheading:17726161... | lld:pubmed |
| pubmed-article:17726161 | pubmed:meshHeading | pubmed-meshheading:17726161... | lld:pubmed |
| pubmed-article:17726161 | pubmed:meshHeading | pubmed-meshheading:17726161... | lld:pubmed |
| pubmed-article:17726161 | pubmed:meshHeading | pubmed-meshheading:17726161... | lld:pubmed |
| pubmed-article:17726161 | pubmed:meshHeading | pubmed-meshheading:17726161... | lld:pubmed |
| pubmed-article:17726161 | pubmed:meshHeading | pubmed-meshheading:17726161... | lld:pubmed |
| pubmed-article:17726161 | pubmed:meshHeading | pubmed-meshheading:17726161... | lld:pubmed |
| pubmed-article:17726161 | pubmed:meshHeading | pubmed-meshheading:17726161... | lld:pubmed |
| pubmed-article:17726161 | pubmed:meshHeading | pubmed-meshheading:17726161... | lld:pubmed |
| pubmed-article:17726161 | pubmed:meshHeading | pubmed-meshheading:17726161... | lld:pubmed |
| pubmed-article:17726161 | pubmed:meshHeading | pubmed-meshheading:17726161... | lld:pubmed |
| pubmed-article:17726161 | pubmed:meshHeading | pubmed-meshheading:17726161... | lld:pubmed |
| pubmed-article:17726161 | pubmed:meshHeading | pubmed-meshheading:17726161... | lld:pubmed |
| pubmed-article:17726161 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:17726161 | pubmed:articleTitle | Excessive exposure to anionic surfaces maintains autoantibody response to beta(2)-glycoprotein I in patients with antiphospholipid syndrome. | lld:pubmed |
| pubmed-article:17726161 | pubmed:affiliation | Division of Rheumatology, Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan. | lld:pubmed |
| pubmed-article:17726161 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17726161 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| entrez-gene:350 | entrezgene:pubmed | pubmed-article:17726161 | lld:entrezgene |
| http://linkedlifedata.com/r... | entrezgene:pubmed | pubmed-article:17726161 | lld:entrezgene |
