Source:http://linkedlifedata.com/resource/pubmed/id/10201893
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
7
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| pubmed:dateCreated |
1999-5-13
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| 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.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Immune Sera,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin G,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin Isotypes,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cholinergic,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interferon,
http://linkedlifedata.com/resource/pubmed/chemical/interferon gamma receptor
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| pubmed:status |
MEDLINE
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| pubmed:month |
Apr
|
| pubmed:issn |
0022-1767
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| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
1
|
| pubmed:volume |
162
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
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| pubmed:pagination |
3775-81
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| pubmed:dateRevised |
2008-11-21
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| pubmed:meshHeading |
pubmed-meshheading:10201893-Animals,
pubmed-meshheading:10201893-Antibody Affinity,
pubmed-meshheading:10201893-Cells, Cultured,
pubmed-meshheading:10201893-Cytokines,
pubmed-meshheading:10201893-Female,
pubmed-meshheading:10201893-Genetic Predisposition to Disease,
pubmed-meshheading:10201893-Immune Sera,
pubmed-meshheading:10201893-Immunization, Passive,
pubmed-meshheading:10201893-Immunoglobulin G,
pubmed-meshheading:10201893-Immunoglobulin Isotypes,
pubmed-meshheading:10201893-Interferon-gamma,
pubmed-meshheading:10201893-Lymphocyte Activation,
pubmed-meshheading:10201893-Mice,
pubmed-meshheading:10201893-Mice, Inbred C57BL,
pubmed-meshheading:10201893-Mice, Knockout,
pubmed-meshheading:10201893-Mice, Transgenic,
pubmed-meshheading:10201893-Muscle Weakness,
pubmed-meshheading:10201893-Myasthenia Gravis,
pubmed-meshheading:10201893-RNA, Messenger,
pubmed-meshheading:10201893-Receptors, Cholinergic,
pubmed-meshheading:10201893-Receptors, Interferon
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| pubmed:year |
1999
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| pubmed:articleTitle |
Mice with IFN-gamma receptor deficiency are less susceptible to experimental autoimmune myasthenia gravis.
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| pubmed:affiliation |
Division of Neurology, Karolinska Institute, Huddinge University Hospital, Stockholm, Sweden. gxzhang@mail.med.upenn.edu
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|