| pubmed-article:20177071 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20177071 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:20177071 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
| pubmed-article:20177071 | lifeskim:mentions | umls-concept:C0033684 | lld:lifeskim |
| pubmed-article:20177071 | lifeskim:mentions | umls-concept:C0947504 | lld:lifeskim |
| pubmed-article:20177071 | lifeskim:mentions | umls-concept:C0971858 | lld:lifeskim |
| pubmed-article:20177071 | lifeskim:mentions | umls-concept:C1538756 | lld:lifeskim |
| pubmed-article:20177071 | lifeskim:mentions | umls-concept:C0332256 | lld:lifeskim |
| pubmed-article:20177071 | lifeskim:mentions | umls-concept:C1553467 | lld:lifeskim |
| pubmed-article:20177071 | lifeskim:mentions | umls-concept:C1511545 | lld:lifeskim |
| pubmed-article:20177071 | pubmed:issue | 16 | lld:pubmed |
| pubmed-article:20177071 | pubmed:dateCreated | 2010-4-12 | lld:pubmed |
| pubmed-article:20177071 | pubmed:abstractText | Rheumatoid arthritis is an autoimmune disease with 1% prevalence in the industrialized world. The contributions of the inflammasome components Nlrp3, ASC, and caspase-1 in the pathogenesis of collagen-induced arthritis have not been characterized. Here, we show that ASC(-/-) mice were protected from arthritis, whereas Nlrp3(-/-) and caspase-1(-/-) mice were susceptible to collagen-induced arthritis. Unlike Nlrp3(-/-) and caspase-1(-/-) mice, the production of collagen-specific antibodies was abolished in ASC(-/-) mice. This was due to a significantly reduced antigen-specific activation of lymphocytes by ASC(-/-) dendritic cells. Antigen-induced proliferation of purified ASC(-/-) T cells was restored upon incubation with wild type dendritic cells, but not when cultured with ASC(-/-) dendritic cells. Moreover, direct T cell receptor ligation with CD3 and CD28 antibodies induced a potent proliferation of ASC(-/-) T cells, indicating that ASC is specifically required in dendritic cells for antigen-induced T cell activation. Therefore, ASC fulfills a hitherto unrecognized inflammasome-independent role in dendritic cells that is crucial for T cell priming and the induction of antigen-specific cellular and humoral immunity and the onset of collagen-induced arthritis. | lld:pubmed |
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| pubmed-article:20177071 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:20177071 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:20177071 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20177071 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:20177071 | pubmed:issn | 1083-351X | lld:pubmed |
| pubmed-article:20177071 | pubmed:author | pubmed-author:BrandDavid... | lld:pubmed |
| pubmed-article:20177071 | pubmed:author | pubmed-author:NeteaMihai... | lld:pubmed |
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| pubmed-article:20177071 | pubmed:author | pubmed-author:LamkanfiMoham... | lld:pubmed |
| pubmed-article:20177071 | pubmed:author | pubmed-author:LuoJiwenJ | lld:pubmed |
| pubmed-article:20177071 | pubmed:author | pubmed-author:StienstraRink... | lld:pubmed |
| pubmed-article:20177071 | pubmed:author | pubmed-author:BoydKelli LKL | lld:pubmed |
| pubmed-article:20177071 | pubmed:author | pubmed-author:KannegantiThi... | lld:pubmed |
| pubmed-article:20177071 | pubmed:author | pubmed-author:IppaguntaSiri... | lld:pubmed |
| pubmed-article:20177071 | pubmed:author | pubmed-author:Van de... | lld:pubmed |
| pubmed-article:20177071 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:20177071 | pubmed:day | 16 | lld:pubmed |
| pubmed-article:20177071 | pubmed:volume | 285 | lld:pubmed |
| pubmed-article:20177071 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:20177071 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:20177071 | pubmed:pagination | 12454-62 | lld:pubmed |
| pubmed-article:20177071 | pubmed:dateRevised | 2011-7-28 | lld:pubmed |
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| pubmed-article:20177071 | pubmed:year | 2010 | lld:pubmed |
| pubmed-article:20177071 | pubmed:articleTitle | Inflammasome-independent role of apoptosis-associated speck-like protein containing a CARD (ASC) in T cell priming is critical for collagen-induced arthritis. | lld:pubmed |
| pubmed-article:20177071 | pubmed:affiliation | Department of Immunology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA. | lld:pubmed |
| pubmed-article:20177071 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:20177071 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:20177071 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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