| pubmed-article:10201893 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10201893 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:10201893 | lifeskim:mentions | umls-concept:C0752087 | lld:lifeskim |
| pubmed-article:10201893 | lifeskim:mentions | umls-concept:C0011155 | lld:lifeskim |
| pubmed-article:10201893 | lifeskim:mentions | umls-concept:C1334197 | lld:lifeskim |
| pubmed-article:10201893 | lifeskim:mentions | umls-concept:C0231204 | lld:lifeskim |
| pubmed-article:10201893 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:10201893 | pubmed:dateCreated | 1999-5-13 | lld:pubmed |
| pubmed-article:10201893 | pubmed:abstractText | IFN-gamma can either adversely or beneficially affect certain experimental autoimmune diseases. To study the role of IFN-gamma in the autoantibody-mediated experimental autoimmune myasthenia gravis (EAMG), an animal model of myasthenia gravis in humans, IFN-gammaR-deficient (IFN-gammaR-/-) mutant C57BL/6 mice and congenic wild-type mice were immunized with Torpedo acetylcholine receptor (AChR) plus CFA. IFN-gammaR-/- mice exhibited significantly lower incidence and severity of muscle weakness, lower anti-AChR IgG Ab levels, and lower Ab affinity to AChR compared with wild-type mice. Passive transfer of serum from IFN-gammaR-/- mice induced less muscular weakness compared with serum from wild-type mice. In contrast, numbers of lymph node cells secreting IFN-gamma and of those expressing IFN-gamma mRNA were strongly augmented in the IFN-gammaR-/- mice, reflecting a failure of negative feedback circuits. Cytokine studies by in situ hybridization revealed lower levels of lymphoid cells expressing AChR-reactive IL-1beta and TNF-alpha mRNA in AChR + CFA-immunized IFN-gammaR-/- mice compared with wild-type mice. No differences were found for AChR-reactive cells expressing IL-4, IL-10, or TGF-beta mRNA. These results indicate that IFN-gamma promotes systemic humoral responses in EAMG by up-regulating the production and the affinity of anti-AChR autoantibodies, thereby contributing to susceptibility to EAMG in C57BL/6-type mice. | lld:pubmed |
| pubmed-article:10201893 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10201893 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10201893 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:10201893 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10201893 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:10201893 | pubmed:issn | 0022-1767 | lld:pubmed |
| pubmed-article:10201893 | pubmed:author | pubmed-author:LindAA | lld:pubmed |
| pubmed-article:10201893 | pubmed:author | pubmed-author:OrrEE | lld:pubmed |
| pubmed-article:10201893 | pubmed:author | pubmed-author:van der... | lld:pubmed |
| pubmed-article:10201893 | pubmed:author | pubmed-author:ZhangG XGX | lld:pubmed |
| pubmed-article:10201893 | pubmed:author | pubmed-author:XiaoB GBG | lld:pubmed |
| pubmed-article:10201893 | pubmed:author | pubmed-author:BaiX FXF | lld:pubmed |
| pubmed-article:10201893 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10201893 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:10201893 | pubmed:volume | 162 | lld:pubmed |
| pubmed-article:10201893 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10201893 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10201893 | pubmed:pagination | 3775-81 | lld:pubmed |
| pubmed-article:10201893 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:10201893 | pubmed:year | 1999 | lld:pubmed |
| pubmed-article:10201893 | pubmed:articleTitle | Mice with IFN-gamma receptor deficiency are less susceptible to experimental autoimmune myasthenia gravis. | lld:pubmed |
| pubmed-article:10201893 | pubmed:affiliation | Division of Neurology, Karolinska Institute, Huddinge University Hospital, Stockholm, Sweden. gxzhang@mail.med.upenn.edu | lld:pubmed |
| pubmed-article:10201893 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10201893 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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