Source:http://linkedlifedata.com/resource/pubmed/id/10229808
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
10
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pubmed:dateCreated |
1999-6-14
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pubmed:abstractText |
Autoantigen administration via nasal mucosal tissue can induce systemic tolerance more effectively than oral administration in a number of experimental autoimmune diseases, including Ab-mediated experimental autoimmune myasthenia gravis, a murine model of myasthenia gravis. The mechanisms underlying nasal tolerance induction are not clear. In this study, we show that nasal administration of acetylcholine receptor (AChR) in C57BL/6 mice, before immunizations with AChR in adjuvant, results in delayed onset and reduced muscle weakness compared with control mice. The delayed onset and reduced muscle weakness were associated with decreased AChR-specific lymphocyte proliferation and decreased levels of anti-AChR Abs of the IgG2a and IgG2b isotypes in serum. The clinical and immunological changes in the AChR-pretreated C57BL/6 wild-type (wt) mice were comparable with those observed in AChR-pretreated CD8-/- mice, indicating that CD8+ T cells were not required for the generation of nasal tolerance. AChR-pretreated wt and CD8-/- mice showed augmented TGF-beta and reduced IFN-gamma responses, whereas levels of IL-4 were unaltered. Splenocytes from AChR-pretreated wt and CD8-/- mice, but not from CD4-/- mice, suppressed AChR-specific lymphocyte proliferation. This suppression could be blocked by Abs against TGF-beta. Thus, our results demonstrate that the suppression induced in the present model is independent of CD8+ T cells and suggest the involvement of Ag-specific CD4+ Th3 cells producing TGF-beta.
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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/Antibodies,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD4,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD8,
http://linkedlifedata.com/resource/pubmed/chemical/Autoantigens,
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cholinergic
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
162
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
5757-63
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:10229808-Animals,
pubmed-meshheading:10229808-Antibodies,
pubmed-meshheading:10229808-Antigens, CD4,
pubmed-meshheading:10229808-Antigens, CD8,
pubmed-meshheading:10229808-Autoantigens,
pubmed-meshheading:10229808-Cytokines,
pubmed-meshheading:10229808-Immune Tolerance,
pubmed-meshheading:10229808-Interferon-gamma,
pubmed-meshheading:10229808-Interleukin-2,
pubmed-meshheading:10229808-Lymphocyte Activation,
pubmed-meshheading:10229808-Mice,
pubmed-meshheading:10229808-Mice, Inbred C57BL,
pubmed-meshheading:10229808-Mice, Mutant Strains,
pubmed-meshheading:10229808-Muscle Weakness,
pubmed-meshheading:10229808-Myasthenia Gravis,
pubmed-meshheading:10229808-Nasal Mucosa,
pubmed-meshheading:10229808-Receptors, Cholinergic,
pubmed-meshheading:10229808-Spleen
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pubmed:year |
1999
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pubmed:articleTitle |
Mechanisms of nasal tolerance induction in experimental autoimmune myasthenia gravis: identification of regulatory cells.
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pubmed:affiliation |
Microbiology and Tumor Biology Center, Karolinska Institutet, Stockholm, Sweden.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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