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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
9
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pubmed:dateCreated |
1997-5-19
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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.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Monoclonal,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD80,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD86,
http://linkedlifedata.com/resource/pubmed/chemical/Cd86 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-4,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0022-1767
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pubmed:author |
pubmed-author:ChenSS,
pubmed-author:FinkelmanF DFD,
pubmed-author:GauseW CWC,
pubmed-author:GreenwaldR JRJ,
pubmed-author:HalvorsonM JMJ,
pubmed-author:LinsleyP SPS,
pubmed-author:LuPP,
pubmed-author:MaddenK BKB,
pubmed-author:MorrisS CSC,
pubmed-author:PeachRR,
pubmed-author:PerrinP JPJ,
pubmed-author:UrbanJ FJFJr,
pubmed-author:ZhouXX
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
158
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
4088-96
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:9126967-Animals,
pubmed-meshheading:9126967-Antibodies, Monoclonal,
pubmed-meshheading:9126967-Antigens, CD,
pubmed-meshheading:9126967-Antigens, CD80,
pubmed-meshheading:9126967-Antigens, CD86,
pubmed-meshheading:9126967-B-Lymphocytes,
pubmed-meshheading:9126967-Cell Differentiation,
pubmed-meshheading:9126967-Cytokines,
pubmed-meshheading:9126967-Eosinophils,
pubmed-meshheading:9126967-Female,
pubmed-meshheading:9126967-Gene Expression,
pubmed-meshheading:9126967-Germinal Center,
pubmed-meshheading:9126967-Immunity, Mucosal,
pubmed-meshheading:9126967-Interleukin-4,
pubmed-meshheading:9126967-Lymphocyte Activation,
pubmed-meshheading:9126967-Mast Cells,
pubmed-meshheading:9126967-Membrane Glycoproteins,
pubmed-meshheading:9126967-Mice,
pubmed-meshheading:9126967-Mice, Inbred BALB C,
pubmed-meshheading:9126967-Nematospiroides dubius,
pubmed-meshheading:9126967-Th2 Cells
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pubmed:year |
1997
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pubmed:articleTitle |
Effects of blocking B7-1 and B7-2 interactions during a type 2 in vivo immune response.
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pubmed:affiliation |
Department of Microbiology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.
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