pubmed-article:11265638 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:11265638 | lifeskim:mentions | umls-concept:C0026896 | lld:lifeskim |
pubmed-article:11265638 | lifeskim:mentions | umls-concept:C0026336 | lld:lifeskim |
pubmed-article:11265638 | lifeskim:mentions | umls-concept:C0021753 | lld:lifeskim |
pubmed-article:11265638 | lifeskim:mentions | umls-concept:C0001041 | lld:lifeskim |
pubmed-article:11265638 | lifeskim:mentions | umls-concept:C0017337 | lld:lifeskim |
pubmed-article:11265638 | lifeskim:mentions | umls-concept:C0301872 | lld:lifeskim |
pubmed-article:11265638 | lifeskim:mentions | umls-concept:C0205216 | lld:lifeskim |
pubmed-article:11265638 | lifeskim:mentions | umls-concept:C0332453 | lld:lifeskim |
pubmed-article:11265638 | lifeskim:mentions | umls-concept:C0591833 | lld:lifeskim |
pubmed-article:11265638 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:11265638 | pubmed:dateCreated | 2001-3-19 | lld:pubmed |
pubmed-article:11265638 | pubmed:abstractText | Human autoimmune myasthenia gravis (MG) is associated with the IL-1beta TaqI RFLP allele 2. Individuals positive for this allele have high levels of inducible IL-1beta in their peripheral blood. Here, we have characterized MG induction and the immune response elicited by Torpedo acetylcholine receptor (AChR) immunization in wild-type and IL-1beta deficient (-/-) mice. Compared with wild-type mice, IL-1beta-/- mice were relatively resistant to induction of clinical experimental autoimmune myasthenia gravis (EAMG). Draining lymph node cells from IL-1beta-/- mice showed poor proliferative capacity upon AChR stimulation in vitro. Both Th1 (IFN-gamma, IL-2) and Th2 (IL-4) cytokine responses were reduced and levels of serum anti-AChR antibodies decreased in IL-1beta-/- mice compared to wild-type mice. Taken together, these results reveal a critical role for IL-1beta in the induction of MG in mice, and support a role for IL-1beta in the pathogenesis of MG in man. | lld:pubmed |
pubmed-article:11265638 | pubmed:language | eng | lld:pubmed |
pubmed-article:11265638 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11265638 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:11265638 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11265638 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11265638 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11265638 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11265638 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:11265638 | pubmed:month | Jan | lld:pubmed |
pubmed-article:11265638 | pubmed:issn | 0014-2980 | lld:pubmed |
pubmed-article:11265638 | pubmed:author | pubmed-author:LefvertA KAK | lld:pubmed |
pubmed-article:11265638 | pubmed:author | pubmed-author:HuangDD | lld:pubmed |
pubmed-article:11265638 | pubmed:author | pubmed-author:ZhouYY | lld:pubmed |
pubmed-article:11265638 | pubmed:author | pubmed-author:GiscombeRR | lld:pubmed |
pubmed-article:11265638 | pubmed:author | pubmed-author:LjunggrenH... | lld:pubmed |
pubmed-article:11265638 | pubmed:author | pubmed-author:GouZ YZY | lld:pubmed |
pubmed-article:11265638 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:11265638 | pubmed:volume | 31 | lld:pubmed |
pubmed-article:11265638 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:11265638 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:11265638 | pubmed:pagination | 225-32 | lld:pubmed |
pubmed-article:11265638 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
pubmed-article:11265638 | pubmed:meshHeading | pubmed-meshheading:11265638... | lld:pubmed |
pubmed-article:11265638 | pubmed:meshHeading | pubmed-meshheading:11265638... | lld:pubmed |
pubmed-article:11265638 | pubmed:meshHeading | pubmed-meshheading:11265638... | lld:pubmed |
pubmed-article:11265638 | pubmed:meshHeading | pubmed-meshheading:11265638... | lld:pubmed |
pubmed-article:11265638 | pubmed:meshHeading | pubmed-meshheading:11265638... | lld:pubmed |
pubmed-article:11265638 | pubmed:meshHeading | pubmed-meshheading:11265638... | lld:pubmed |
pubmed-article:11265638 | pubmed:meshHeading | pubmed-meshheading:11265638... | lld:pubmed |
pubmed-article:11265638 | pubmed:meshHeading | pubmed-meshheading:11265638... | lld:pubmed |
pubmed-article:11265638 | pubmed:meshHeading | pubmed-meshheading:11265638... | lld:pubmed |
pubmed-article:11265638 | pubmed:meshHeading | pubmed-meshheading:11265638... | lld:pubmed |
pubmed-article:11265638 | pubmed:year | 2001 | lld:pubmed |
pubmed-article:11265638 | pubmed:articleTitle | Disruption of the IL-1beta gene diminishes acetylcholine receptor-induced immune responses in a murine model of myasthenia gravis. | lld:pubmed |
pubmed-article:11265638 | pubmed:affiliation | Department of Neurosciences NC30, The Lerner ResearchInstitute, Cleveland Clinic Foundation, 9500-10000 Euclid Avenue, Cleveland, OH 44195, USA. huangd2@ccf.org | lld:pubmed |
pubmed-article:11265638 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:11265638 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
entrez-gene:16176 | entrezgene:pubmed | pubmed-article:11265638 | lld:entrezgene |