pubmed-article:9126967 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:9126967 | lifeskim:mentions | umls-concept:C0332307 | lld:lifeskim |
pubmed-article:9126967 | lifeskim:mentions | umls-concept:C2698599 | lld:lifeskim |
pubmed-article:9126967 | lifeskim:mentions | umls-concept:C0104998 | lld:lifeskim |
pubmed-article:9126967 | lifeskim:mentions | umls-concept:C1704675 | lld:lifeskim |
pubmed-article:9126967 | lifeskim:mentions | umls-concept:C1280500 | lld:lifeskim |
pubmed-article:9126967 | lifeskim:mentions | umls-concept:C0301872 | lld:lifeskim |
pubmed-article:9126967 | lifeskim:mentions | umls-concept:C1705431 | lld:lifeskim |
pubmed-article:9126967 | lifeskim:mentions | umls-concept:C0332206 | lld:lifeskim |
pubmed-article:9126967 | lifeskim:mentions | umls-concept:C1515655 | lld:lifeskim |
pubmed-article:9126967 | pubmed:issue | 9 | lld:pubmed |
pubmed-article:9126967 | pubmed:dateCreated | 1997-5-19 | lld:pubmed |
pubmed-article:9126967 | pubmed:abstractText | The costimulatory signal provided to T cells through CD28/CTLA-4 interactions is required for in vivo Th cell effector function associated with cytokine production. However, it is uncertain whether the two well-characterized ligands for these molecules, B7-1 and B7-2, differentially influence the consequent development of a type 1 or a type 2 primary response. We have examined the in vivo effects of blocking B7-1 and/or B7-2 ligand interactions on the type 2 mucosal immune response that follows oral infection of mice with the nematode parasite, Heligmosomoides polygyrus. Administration of the combination of anti-B7-1 and anti-B7-2 Abs inhibited H. polygyrus-induced increases in serum IgG1 and IgE levels, the expansion of mesenteric lymph node (MLN) germinal centers, in situ CD4+ T cell expansion, elevated blood eosinophils, and increased intestinal mucosal mast cells. Similarly, both Abs blocked MLN and Peyer's patch cytokine gene expression and elevations in MLN T cell-derived IL-4 protein secretion. However, in the same experiments, administration of either anti-B7-1 or anti-B7-2 Abs alone had little effect on any of these parameters. T cell and B cell activation was also blocked by the combination of anti-B7-2 and a B7-1-specific mutant Y100F CTLA-4Ig construct. These results suggest that to the extent that anti-B7-1 and anti-B7-2 mAbs block B7 interactions, either B7-1 or B7-2 ligand interactions can provide the required costimulatory signals that lead to T cell effector function during a type 2 in vivo immune response. | lld:pubmed |
pubmed-article:9126967 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9126967 | pubmed:language | eng | lld:pubmed |
pubmed-article:9126967 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9126967 | pubmed:citationSubset | AIM | lld:pubmed |
pubmed-article:9126967 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:9126967 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9126967 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9126967 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:9126967 | pubmed:month | May | lld:pubmed |
pubmed-article:9126967 | pubmed:issn | 0022-1767 | lld:pubmed |
pubmed-article:9126967 | pubmed:author | pubmed-author:ChenSS | lld:pubmed |
pubmed-article:9126967 | pubmed:author | pubmed-author:FinkelmanF... | lld:pubmed |
pubmed-article:9126967 | pubmed:author | pubmed-author:MorrisS CSC | lld:pubmed |
pubmed-article:9126967 | pubmed:author | pubmed-author:ZhouXX | lld:pubmed |
pubmed-article:9126967 | pubmed:author | pubmed-author:LinsleyP SPS | lld:pubmed |
pubmed-article:9126967 | pubmed:author | pubmed-author:LuPP | lld:pubmed |
pubmed-article:9126967 | pubmed:author | pubmed-author:UrbanJ FJFJr | lld:pubmed |
pubmed-article:9126967 | pubmed:author | pubmed-author:PeachRR | lld:pubmed |
pubmed-article:9126967 | pubmed:author | pubmed-author:GauseW CWC | lld:pubmed |
pubmed-article:9126967 | pubmed:author | pubmed-author:MaddenK BKB | lld:pubmed |
pubmed-article:9126967 | pubmed:author | pubmed-author:HalvorsonM... | lld:pubmed |
pubmed-article:9126967 | pubmed:author | pubmed-author:PerrinP JPJ | lld:pubmed |
pubmed-article:9126967 | pubmed:author | pubmed-author:GreenwaldR... | lld:pubmed |
pubmed-article:9126967 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:9126967 | pubmed:day | 1 | lld:pubmed |
pubmed-article:9126967 | pubmed:volume | 158 | lld:pubmed |
pubmed-article:9126967 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:9126967 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:9126967 | pubmed:pagination | 4088-96 | lld:pubmed |
pubmed-article:9126967 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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pubmed-article:9126967 | pubmed:meshHeading | pubmed-meshheading:9126967-... | lld:pubmed |
pubmed-article:9126967 | pubmed:year | 1997 | lld:pubmed |
pubmed-article:9126967 | pubmed:articleTitle | Effects of blocking B7-1 and B7-2 interactions during a type 2 in vivo immune response. | lld:pubmed |
pubmed-article:9126967 | pubmed:affiliation | Department of Microbiology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA. | lld:pubmed |
pubmed-article:9126967 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:9126967 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:9126967 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
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