| pubmed-article:19124760 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19124760 | lifeskim:mentions | umls-concept:C0014072 | lld:lifeskim |
| pubmed-article:19124760 | lifeskim:mentions | umls-concept:C0245382 | lld:lifeskim |
| pubmed-article:19124760 | lifeskim:mentions | umls-concept:C0439793 | lld:lifeskim |
| pubmed-article:19124760 | lifeskim:mentions | umls-concept:C0011155 | lld:lifeskim |
| pubmed-article:19124760 | lifeskim:mentions | umls-concept:C0392756 | lld:lifeskim |
| pubmed-article:19124760 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:19124760 | pubmed:dateCreated | 2009-1-6 | lld:pubmed |
| pubmed-article:19124760 | 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. | lld:pubmed |
| pubmed-article:19124760 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19124760 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19124760 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19124760 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:19124760 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19124760 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:19124760 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19124760 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:19124760 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19124760 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19124760 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:19124760 | pubmed:issn | 1550-6606 | lld:pubmed |
| pubmed-article:19124760 | pubmed:author | pubmed-author:LiuFu-TongFT | lld:pubmed |
| pubmed-article:19124760 | pubmed:author | pubmed-author:XuDamoD | lld:pubmed |
| pubmed-article:19124760 | pubmed:author | pubmed-author:LiewFoo YFY | lld:pubmed |
| pubmed-article:19124760 | pubmed:author | pubmed-author:GoodyearCarl... | lld:pubmed |
| pubmed-article:19124760 | pubmed:author | pubmed-author:LukicMiodrag... | lld:pubmed |
| pubmed-article:19124760 | pubmed:author | pubmed-author:JiangHui-Rong... | lld:pubmed |
| pubmed-article:19124760 | pubmed:author | pubmed-author:ShahinAllenA | lld:pubmed |
| pubmed-article:19124760 | pubmed:author | pubmed-author:FukadaSandra... | lld:pubmed |
| pubmed-article:19124760 | pubmed:author | pubmed-author:Mensah-BrownE... | lld:pubmed |
| pubmed-article:19124760 | pubmed:author | pubmed-author:Al... | lld:pubmed |
| pubmed-article:19124760 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19124760 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:19124760 | pubmed:volume | 182 | lld:pubmed |
| pubmed-article:19124760 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19124760 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19124760 | pubmed:pagination | 1167-73 | lld:pubmed |
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| pubmed-article:19124760 | pubmed:year | 2009 | lld:pubmed |
| pubmed-article:19124760 | pubmed:articleTitle | Galectin-3 deficiency reduces the severity of experimental autoimmune encephalomyelitis. | lld:pubmed |
| pubmed-article:19124760 | pubmed:affiliation | Division of Immunology, Infection and Inflammation, Glasgow Biomedical Research Centre, University of Glasgow, Glasgow, UK. | lld:pubmed |
| pubmed-article:19124760 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:19124760 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| entrez-gene:16854 | entrezgene:pubmed | pubmed-article:19124760 | lld:entrezgene |
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