Source:http://linkedlifedata.com/resource/pubmed/id/19124760
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
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| pubmed:dateCreated |
2009-1-6
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| pubmed:abstractText |
Galectin-3 (Gal-3) is a member of the beta-galactoside-binding lectin family and plays an important role in inflammation. However, the precise role of Gal-3 in autoimmune diseases remains obscure. We have investigated the functional role of Gal-3 in experimental autoimmune encephalomyelitis (EAE) following immunization with myelin oligodendrocyte glycoprotein (MOG)35-55 peptide. Gal-3 deficient (Gal-3-/-) mice developed significantly milder EAE and markedly reduced leukocyte infiltration in the CNS compared with similarly treated wild-type (WT) mice. Gal-3-/- mice also contained fewer monocytes and macrophages but more apoptotic cells in the CNS than did WT mice. Following Ag stimulation in vitro, lymph node cells from the immunized Gal-3-/- mice produced less IL-17 and IFN-gamma than did those of the WT mice. In contrast, Gal-3-/- mice produced more serum IL-10, IL-5, and IL-13 and contained higher frequency of Foxp3+ regulatory T cells in the CNS than did the WT mice. Furthermore, bone marrow-derived dendritic cells from Gal-3-/- mice produced more IL-10 in response to LPS or bacterial lipoprotein than did WT marrow-derived dendritic cells. Moreover, Gal-3-/- dendritic cells induced Ag-specific T cells to produce more IL-10, IL-5, and IL-12, but less IL-17, than did WT dendritic cells. Taken together, our data demonstrate that Gal-3 plays an important disease-exacerbating role in EAE through its multifunctional roles in preventing cell apoptosis and increasing IL-17 and IFN-gamma synthesis, but decreasing IL-10 production.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Galectin 3,
http://linkedlifedata.com/resource/pubmed/chemical/Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Growth Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-10,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-17,
http://linkedlifedata.com/resource/pubmed/chemical/Peptide Fragments,
http://linkedlifedata.com/resource/pubmed/chemical/myelin oligodendrocyte...
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| pubmed:status |
MEDLINE
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| pubmed:month |
Jan
|
| pubmed:issn |
1550-6606
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| pubmed:author | |
| pubmed:issnType |
Electronic
|
| pubmed:day |
15
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| pubmed:volume |
182
|
| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
1167-73
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| pubmed:meshHeading |
pubmed-meshheading:19124760-Animals,
pubmed-meshheading:19124760-Apoptosis,
pubmed-meshheading:19124760-Cells, Cultured,
pubmed-meshheading:19124760-Central Nervous System,
pubmed-meshheading:19124760-Down-Regulation,
pubmed-meshheading:19124760-Encephalomyelitis, Autoimmune, Experimental,
pubmed-meshheading:19124760-Galectin 3,
pubmed-meshheading:19124760-Glycoproteins,
pubmed-meshheading:19124760-Growth Inhibitors,
pubmed-meshheading:19124760-Interleukin-10,
pubmed-meshheading:19124760-Interleukin-17,
pubmed-meshheading:19124760-Male,
pubmed-meshheading:19124760-Mice,
pubmed-meshheading:19124760-Mice, Inbred C57BL,
pubmed-meshheading:19124760-Mice, Knockout,
pubmed-meshheading:19124760-Mice, Transgenic,
pubmed-meshheading:19124760-Peptide Fragments,
pubmed-meshheading:19124760-Severity of Illness Index,
pubmed-meshheading:19124760-Up-Regulation
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| pubmed:year |
2009
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| pubmed:articleTitle |
Galectin-3 deficiency reduces the severity of experimental autoimmune encephalomyelitis.
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| pubmed:affiliation |
Division of Immunology, Infection and Inflammation, Glasgow Biomedical Research Centre, University of Glasgow, Glasgow, UK.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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