Linked Life Data

11358460

Source:http://linkedlifedata.com/resource/pubmed/id/11358460

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2001-5-18
pubmed:abstractText
Experimental autoimmune neuritis (EAN) is an animal model of the human disease Guillain-Barré syndrome. In this autoimmune inflammatory disease, CD4(+) T cells mediate demyelination in the peripheral nervous system (PNS). Infiltrating macrophages and T cells as well as cytokines like interferon (IFN)-gamma are intimately involved in causing pathogenic effects. To investigate the role of IFN-gamma in cell-mediated EAN, IFN-gamma receptor-deficient mutant (IFN-gammaR(-/-)) C57BL/6 mice and corresponding wild-type mice were immunized with P0 peptide 180-199, a purified component of peripheral nerve myelin, and Freund's complete adjuvant. IFN-gammaR(-/-) mice exhibited later onset of clinical disease. The disease was also less severe than in wild-type mice. Fewer IL-12-producing but more IL-4-producing cells were found in sciatic nerve sections from IFN-gammaR(-/-) mice than from wild-type mice on day 24 postimmunization, i.e., at the peak of clinical EAN. At the same time, IFN-gammaR(-/-) mice had less infiltration of inflammatory cells, including macrophages, CD4(+) T cells, and monocytes, into sciatic nerve tissue and less demyelination. However, numbers of IFN-gamma-secreting cells from the spleen were significantly augmented in the IFN-gammaR(-/-) mice, reflecting a failure of negative feedback circuits. The IFN-gammaR deficiency did not affect the production of anti-P0 peptide 180-199-specific antibodies. These results indicate that IFN-gamma contributes to a susceptibility for EAN in C57BL/6 mice by promoting a Th1 cell-mediated immune response and suppressing a Th2 response.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0014-4886
pubmed:author
pubmed:copyrightInfo
Copyright 2001 Academic Press.
pubmed:issnType
Print
pubmed:volume
169
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
472-8
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:11358460-Animals, pubmed-meshheading:11358460-CD4-Positive T-Lymphocytes, pubmed-meshheading:11358460-Disease Progression, pubmed-meshheading:11358460-Feedback, pubmed-meshheading:11358460-Freund's Adjuvant, pubmed-meshheading:11358460-Humans, pubmed-meshheading:11358460-Inflammation, pubmed-meshheading:11358460-Interferon-gamma, pubmed-meshheading:11358460-Interleukin-12, pubmed-meshheading:11358460-Interleukin-4, pubmed-meshheading:11358460-Macrophages, pubmed-meshheading:11358460-Mice, pubmed-meshheading:11358460-Mice, Inbred C57BL, pubmed-meshheading:11358460-Mice, Knockout, pubmed-meshheading:11358460-Monocytes, pubmed-meshheading:11358460-Myelin P0 Protein, pubmed-meshheading:11358460-Neuritis, Autoimmune, Experimental, pubmed-meshheading:11358460-Peptide Fragments, pubmed-meshheading:11358460-Receptors, Interferon, pubmed-meshheading:11358460-Sciatic Nerve
pubmed:year
2001
pubmed:articleTitle
Suppression of autoimmune neuritis in IFN-gamma receptor-deficient mice.
pubmed:affiliation
Division of Geriatric Medicine, Department of Clinical Neuroscience, Karolinska Institute, Huddinge University Hospital, S-141 86 Stockholm, Sweden.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't