Linked Life Data

16415102

Source:http://linkedlifedata.com/resource/pubmed/id/16415102

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2006-1-26
pubmed:abstractText
IL-1 is a pro-inflammatory cytokine that plays an important role in inflammation and host responses to infection. We have previously shown that imbalances in the IL-1 and IL-1R antagonist (IL-1Ra) system cause the development of inflammatory diseases. To explore the role of the IL-1/IL-1Ra system in autoimmune disease, we analyzed myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) in mice bearing targeted disruptions of the IL-1alpha, IL-1beta, IL-1alpha and IL-1beta (IL-1) or IL-1Ra genes. IL-1alpha/beta double-deficient (IL-1-/-) mice exhibited significant resistance to EAE induction with a significant reduction in disease severity, while IL-1alpha-/- or IL-1beta-/- mice developed EAE in a manner similar to wild-type mice. IL-1Ra-/- mice also developed MOG-induced EAE normally with pertussis toxin (PTx) administration. In contrast to wild-type mice, however, these mice were highly susceptible to EAE induction in the absence of PTx administration. We found that both IFN-gamma and IL-17 production and proliferation were reduced in IL-1-/- T cells upon stimulation with MOG, while IFN-gamma, IL-17 and tumor necrosis factor-alpha production and proliferation were enhanced in IL-1Ra-/- T cells. These observations suggest that the IL-1/IL-1Ra system is crucial for auto-antigen-specific T cell induction and contributes to the development of EAE.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0953-8178
pubmed:author
pubmed:issnType
Print
pubmed:volume
18
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
399-407
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:16415102-Amino Acid Sequence, pubmed-meshheading:16415102-Animals, pubmed-meshheading:16415102-Encephalomyelitis, Autoimmune, Experimental, pubmed-meshheading:16415102-Epitopes, pubmed-meshheading:16415102-Female, pubmed-meshheading:16415102-Interleukin 1 Receptor Antagonist Protein, pubmed-meshheading:16415102-Interleukin-1, pubmed-meshheading:16415102-Lymphocyte Activation, pubmed-meshheading:16415102-Male, pubmed-meshheading:16415102-Mice, pubmed-meshheading:16415102-Mice, Inbred C57BL, pubmed-meshheading:16415102-Molecular Sequence Data, pubmed-meshheading:16415102-Myelin Proteins, pubmed-meshheading:16415102-Myelin-Associated Glycoprotein, pubmed-meshheading:16415102-Receptors, Interleukin-1, pubmed-meshheading:16415102-Sialoglycoproteins, pubmed-meshheading:16415102-T-Lymphocytes
pubmed:year
2006
pubmed:articleTitle
Abnormal T cell activation caused by the imbalance of the IL-1/IL-1R antagonist system is responsible for the development of experimental autoimmune encephalomyelitis.
pubmed:affiliation
Center for Experimental Medicine, Institute of Medical Science, University of Tokyo, Minato-ku, Tokyo 108-8639, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't