| pubmed-article:20007589 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20007589 | lifeskim:mentions | umls-concept:C0003873 | lld:lifeskim |
| pubmed-article:20007589 | lifeskim:mentions | umls-concept:C0006751 | lld:lifeskim |
| pubmed-article:20007589 | lifeskim:mentions | umls-concept:C0034790 | lld:lifeskim |
| pubmed-article:20007589 | lifeskim:mentions | umls-concept:C0449864 | lld:lifeskim |
| pubmed-article:20007589 | pubmed:issue | 12 | lld:pubmed |
| pubmed-article:20007589 | pubmed:dateCreated | 2009-12-16 | lld:pubmed |
| pubmed-article:20007589 | pubmed:abstractText | Immune responses to citrullinated neoantigens and clinical efficacy of costimulation blockade indicate a general defect in maintaining T cell tolerance in rheumatoid arthritis (RA). To examine whether TCR threshold calibration contributes to disease pathogenesis, signaling in RA T cells was quantified. RA patients had a selective increase in ERK phosphorylation compared with demographically matched controls due to a mechanism distal of Ras activation. Increased ERK responses included naive and memory CD4 and CD8 T cells and did not correlate with disease activity. The augmented ERK activity delayed SHP-1 recruitment to the TCR synapse and sustained TCR-induced Zap70 and NF-kappaB signaling, facilitating responses to suboptimal stimulation. Increased responsiveness of the ERK pathway was also a characteristic finding in the SKG mouse model of RA where it preceded clinical symptoms. Treatment with subtherapeutic doses of a MEK-1/2 inhibitor delayed arthritis onset and reduced severity, suggesting that increased ERK phosphorylation predisposes for autoimmunity and can be targeted to prevent disease. | lld:pubmed |
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| pubmed-article:20007589 | pubmed:language | eng | lld:pubmed |
| pubmed-article:20007589 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20007589 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:20007589 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20007589 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:20007589 | pubmed:issn | 1550-6606 | lld:pubmed |
| pubmed-article:20007589 | pubmed:author | pubmed-author:WeyandCorneli... | lld:pubmed |
| pubmed-article:20007589 | pubmed:author | pubmed-author:GoronzyJörg... | lld:pubmed |
| pubmed-article:20007589 | pubmed:author | pubmed-author:SinghKarnailK | lld:pubmed |
| pubmed-article:20007589 | pubmed:author | pubmed-author:ColmegnaInésI | lld:pubmed |
| pubmed-article:20007589 | pubmed:author | pubmed-author:PryshchepSerg... | lld:pubmed |
| pubmed-article:20007589 | pubmed:author | pubmed-author:DeshpandePrat... | lld:pubmed |
| pubmed-article:20007589 | pubmed:author | pubmed-author:LiarskiVladim... | lld:pubmed |
| pubmed-article:20007589 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:20007589 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:20007589 | pubmed:volume | 183 | lld:pubmed |
| pubmed-article:20007589 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:20007589 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:20007589 | pubmed:pagination | 8258-67 | lld:pubmed |
| pubmed-article:20007589 | pubmed:dateRevised | 2011-1-5 | lld:pubmed |
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