pubmed-article:17982081 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:17982081 | lifeskim:mentions | umls-concept:C0242632 | lld:lifeskim |
pubmed-article:17982081 | lifeskim:mentions | umls-concept:C0011306 | lld:lifeskim |
pubmed-article:17982081 | lifeskim:mentions | umls-concept:C0023693 | lld:lifeskim |
pubmed-article:17982081 | lifeskim:mentions | umls-concept:C1704632 | lld:lifeskim |
pubmed-article:17982081 | lifeskim:mentions | umls-concept:C0871261 | lld:lifeskim |
pubmed-article:17982081 | lifeskim:mentions | umls-concept:C1332714 | lld:lifeskim |
pubmed-article:17982081 | lifeskim:mentions | umls-concept:C1420817 | lld:lifeskim |
pubmed-article:17982081 | lifeskim:mentions | umls-concept:C2911692 | lld:lifeskim |
pubmed-article:17982081 | lifeskim:mentions | umls-concept:C1706817 | lld:lifeskim |
pubmed-article:17982081 | lifeskim:mentions | umls-concept:C1819439 | lld:lifeskim |
pubmed-article:17982081 | lifeskim:mentions | umls-concept:C0683598 | lld:lifeskim |
pubmed-article:17982081 | lifeskim:mentions | umls-concept:C0023276 | lld:lifeskim |
pubmed-article:17982081 | lifeskim:mentions | umls-concept:C1511545 | lld:lifeskim |
pubmed-article:17982081 | lifeskim:mentions | umls-concept:C2698651 | lld:lifeskim |
pubmed-article:17982081 | pubmed:issue | 10 | lld:pubmed |
pubmed-article:17982081 | pubmed:dateCreated | 2007-11-5 | lld:pubmed |
pubmed-article:17982081 | pubmed:abstractText | Although studies indicate LIGHT (lymphotoxin (LT)-like, exhibits inducible expression and competes with HSV glycoprotein D for herpes virus entry mediator (HVEM), a receptor expressed by T lymphocytes) enhances inflammation and T cell-mediated immunity, the mechanisms involved in this process remain obscure. In this study, we assessed the role of LIGHT in IL-12 production and development of CD4(+) Th cells type one (Th1) in vivo. Bone marrow-derived dendritic cells from LIGHT(-/-) mice were severely impaired in IL-12p40 production following IFN-gamma and LPS stimulation in vitro. Furthermore, blockade of LIGHT in vitro and in vivo with HVEM-Ig and LT beta receptor (LTbetaR)-Ig leads to impaired IL-12 production and defective polyclonal and Ag-specific IFN-gamma production in vivo. In an infection model, injection of HVEM-Ig or LTbetaR-Ig into the usually resistant C57BL/6 mice results in defective IL-12 and IFN-gamma production and severe susceptibility to Leishmania major that was reversed by rIL-12 treatment. This striking susceptibility to L. major in mice injected with HVEM-Ig or LTbetaR-Ig was also reproduced in LIGHT(-/-) --> RAG1(-/-) chimeric mice. In contrast, L. major-infected LTbeta(-/-) mice do not develop acute disease, suggesting that the effect of LTbetaR-Ig is not due to blockade of membrane LT (LTalpha1beta2) signaling. Collectively, our data show that LIGHT plays a critical role for optimal IL-12 production by DC and the development of IFN-gamma-producing CD4(+) Th1 cells and its blockade results in severe susceptibility to Leishmania major. | lld:pubmed |
pubmed-article:17982081 | pubmed:language | eng | lld:pubmed |
pubmed-article:17982081 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17982081 | pubmed:citationSubset | AIM | lld:pubmed |
pubmed-article:17982081 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:17982081 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17982081 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17982081 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:17982081 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:17982081 | pubmed:month | Nov | lld:pubmed |
pubmed-article:17982081 | pubmed:issn | 0022-1767 | lld:pubmed |
pubmed-article:17982081 | pubmed:author | pubmed-author:WangYangY | lld:pubmed |
pubmed-article:17982081 | pubmed:author | pubmed-author:FuYang-XinYX | lld:pubmed |
pubmed-article:17982081 | pubmed:author | pubmed-author:LiuDongD | lld:pubmed |
pubmed-article:17982081 | pubmed:author | pubmed-author:XuGuilianG | lld:pubmed |
pubmed-article:17982081 | pubmed:author | pubmed-author:UzonnaJude... | lld:pubmed |
pubmed-article:17982081 | pubmed:author | pubmed-author:KornerHeinric... | lld:pubmed |
pubmed-article:17982081 | pubmed:author | pubmed-author:KungSam K PSK | lld:pubmed |
pubmed-article:17982081 | pubmed:author | pubmed-author:OkworIfeomaI | lld:pubmed |
pubmed-article:17982081 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:17982081 | pubmed:day | 15 | lld:pubmed |
pubmed-article:17982081 | pubmed:volume | 179 | lld:pubmed |
pubmed-article:17982081 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:17982081 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:17982081 | pubmed:pagination | 6901-9 | lld:pubmed |
pubmed-article:17982081 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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pubmed-article:17982081 | pubmed:year | 2007 | lld:pubmed |
pubmed-article:17982081 | pubmed:articleTitle | LIGHT Is critical for IL-12 production by dendritic cells, optimal CD4+ Th1 cell response, and resistance to Leishmania major. | lld:pubmed |
pubmed-article:17982081 | pubmed:affiliation | Department of Immunology, Faculty of Medicine University of Manitoba, Winnipeg, Canada. | lld:pubmed |
pubmed-article:17982081 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:17982081 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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