| pubmed-article:10878575 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10878575 | lifeskim:mentions | umls-concept:C0007587 | lld:lifeskim |
| pubmed-article:10878575 | lifeskim:mentions | umls-concept:C0004368 | lld:lifeskim |
| pubmed-article:10878575 | lifeskim:mentions | umls-concept:C1444748 | lld:lifeskim |
| pubmed-article:10878575 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:10878575 | pubmed:dateCreated | 2000-10-3 | lld:pubmed |
| pubmed-article:10878575 | pubmed:abstractText | Systemic autoimmune diseases are characterized by the production of antibodies against a broad range of self-antigens. Recent evidence indicates that the majority of these autoantigens are modified in various ways during cell death. This has led to the hypothesis that the primary immune response in the development of autoimmunity is directed to components of the dying cell. In this article, we summarize data on the modification of autoantigens during cell death and the possible consequences of this for autoimmunity. | lld:pubmed |
| pubmed-article:10878575 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10878575 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10878575 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:10878575 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10878575 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10878575 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10878575 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:10878575 | pubmed:issn | 0265-9247 | lld:pubmed |
| pubmed-article:10878575 | pubmed:author | pubmed-author:van... | lld:pubmed |
| pubmed-article:10878575 | pubmed:author | pubmed-author:RodenburgR... | lld:pubmed |
| pubmed-article:10878575 | pubmed:author | pubmed-author:PruijnG JGJ | lld:pubmed |
| pubmed-article:10878575 | pubmed:author | pubmed-author:RaatsJ MJM | lld:pubmed |
| pubmed-article:10878575 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10878575 | pubmed:volume | 22 | lld:pubmed |
| pubmed-article:10878575 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10878575 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10878575 | pubmed:pagination | 627-36 | lld:pubmed |
| pubmed-article:10878575 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:10878575 | pubmed:meshHeading | pubmed-meshheading:10878575... | lld:pubmed |
| pubmed-article:10878575 | pubmed:meshHeading | pubmed-meshheading:10878575... | lld:pubmed |
| pubmed-article:10878575 | pubmed:meshHeading | pubmed-meshheading:10878575... | lld:pubmed |
| pubmed-article:10878575 | pubmed:meshHeading | pubmed-meshheading:10878575... | lld:pubmed |
| pubmed-article:10878575 | pubmed:year | 2000 | lld:pubmed |
| pubmed-article:10878575 | pubmed:articleTitle | Cell death: a trigger of autoimmunity? | lld:pubmed |
| pubmed-article:10878575 | pubmed:affiliation | Department of Biochemistry, University of Nijmegen, The Netherlands. | lld:pubmed |
| pubmed-article:10878575 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10878575 | pubmed:publicationType | Review | lld:pubmed |
| pubmed-article:10878575 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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