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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
12
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pubmed:dateCreated |
2001-10-19
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pubmed:abstractText |
Interleukin-18 (IL-18) is a pleiotropic proinflammatory cytokine that plays an important role in interferon gamma (IFN-gamma) production and IL-12-driven Th1 phenotype polarization. Increased expression of IL-18 has been observed in several autoimmune diseases. In this study we have analyzed the role of IL-18 in an antibody-mediated autoimmune disease and elucidated the mechanisms involved in disease suppression mediated by blockade of IL-18, using experimental autoimmune myasthenia gravis (EAMG) as a model. EAMG is a T cell-regulated, antibody-mediated autoimmune disease in which the nicotinic acetylcholine receptor (AChR) is the major autoantigen. Th1- and Th2-type responses are both implicated in EAMG development. We show that treatment by anti-IL-18 during ongoing EAMG suppresses disease progression. The protective effect can be adoptively transferred to naive recipients and is mediated by increased levels of the immunosuppressive Th3-type cytokine TGF-beta and decreased AChR-specific Th1-type cellular responses. Suppression of EAMG is accompanied by down-regulation of the costimulatory factor CD40L and up-regulation of CTLA-4, a key negative immunomodulator. Our results suggest that IL-18 blockade may potentially be applied for immunointervention in myasthenia gravis.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Differentiation,
http://linkedlifedata.com/resource/pubmed/chemical/CD40 Ligand,
http://linkedlifedata.com/resource/pubmed/chemical/CTLA-4 Antigen,
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoconjugates,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin G,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-18,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Nicotinic,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta,
http://linkedlifedata.com/resource/pubmed/chemical/abatacept
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
1530-6860
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:volume |
15
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2140-8
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:11641240-Animals,
pubmed-meshheading:11641240-Antibodies,
pubmed-meshheading:11641240-Antigens, CD,
pubmed-meshheading:11641240-Antigens, Differentiation,
pubmed-meshheading:11641240-B-Lymphocytes,
pubmed-meshheading:11641240-CD40 Ligand,
pubmed-meshheading:11641240-CTLA-4 Antigen,
pubmed-meshheading:11641240-Cells, Cultured,
pubmed-meshheading:11641240-Cytokines,
pubmed-meshheading:11641240-Disease Progression,
pubmed-meshheading:11641240-Female,
pubmed-meshheading:11641240-Hypersensitivity, Delayed,
pubmed-meshheading:11641240-Immunoconjugates,
pubmed-meshheading:11641240-Immunoglobulin G,
pubmed-meshheading:11641240-Interleukin-18,
pubmed-meshheading:11641240-Kinetics,
pubmed-meshheading:11641240-Lymphocyte Activation,
pubmed-meshheading:11641240-Myasthenia Gravis, Autoimmune, Experimental,
pubmed-meshheading:11641240-Rats,
pubmed-meshheading:11641240-Rats, Inbred Lew,
pubmed-meshheading:11641240-Receptors, Nicotinic,
pubmed-meshheading:11641240-T-Lymphocytes,
pubmed-meshheading:11641240-Th1 Cells,
pubmed-meshheading:11641240-Transforming Growth Factor beta
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pubmed:year |
2001
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pubmed:articleTitle |
Suppression of experimental myasthenia gravis, a B cell-mediated autoimmune disease, by blockade of IL-18.
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pubmed:affiliation |
Department of Immunology, The Weizmann Institute of Science, Rehovot 76100, Israel.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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