| pubmed-article:8921434 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8921434 | lifeskim:mentions | umls-concept:C2698599 | lld:lifeskim |
| pubmed-article:8921434 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
| pubmed-article:8921434 | lifeskim:mentions | umls-concept:C1413243 | lld:lifeskim |
| pubmed-article:8921434 | lifeskim:mentions | umls-concept:C1527148 | lld:lifeskim |
| pubmed-article:8921434 | lifeskim:mentions | umls-concept:C0205224 | lld:lifeskim |
| pubmed-article:8921434 | pubmed:issue | 10 | lld:pubmed |
| pubmed-article:8921434 | pubmed:dateCreated | 1997-2-10 | lld:pubmed |
| pubmed-article:8921434 | pubmed:abstractText | The CD28/CTLA-4 ligands, B7-1 (CD80) and B7-2 (CD86), provide a co-stimulatory signal necessary for optimal T cell activation. We have examined the effect of blocking B7-1 and B7-2 in an in vitro system using ovalbumin-specific T cells from alpha beta TCR-transgenic mice. This system allowed us to examine the interaction of B7 co-stimulators on physiologic antigen-presenting cells (APC) with antigen-specific T helper precursor (ThP) cells. We report that blocking Thp/B7-1 or B7-2 interactions in a primary response differentially affects the cytokine profile observed in a secondary stimulation, even in the absence of additional anti-B7 antibody. Engagement of B7-2 in the primary stimulation was found to be essential for production of the Th2 cytokine, IL-4, but not the Th1 cytokines, IL-2 and IFN-gamma, in a secondary stimulation. Conversely, inclusion of the anti-B7-1 mAb in cultures using highly purified naive T cells increased levels of IL-4 and significantly depressed levels of IFN-gamma, upon re-stimulation. The effect of the anti-B7-2 mAb in reducing IL-4 production could be overcome by the addition of recombinant IL-4 in the primary stimulation. The effects of the anti-B7-2 mAb appear to be due to blocking and not cross-linking, as F(ab) fragments mimicked the intact antibody. Taken together, our data demonstrate that the interaction between Thp and B7-2 favors the development of Th2 cells. | lld:pubmed |
| pubmed-article:8921434 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8921434 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8921434 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:8921434 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8921434 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:8921434 | pubmed:issn | 0953-8178 | lld:pubmed |
| pubmed-article:8921434 | pubmed:author | pubmed-author:DayM JMJ | lld:pubmed |
| pubmed-article:8921434 | pubmed:author | pubmed-author:GlimcherL HLH | lld:pubmed |
| pubmed-article:8921434 | pubmed:author | pubmed-author:KuchrooV KVK | lld:pubmed |
| pubmed-article:8921434 | pubmed:author | pubmed-author:RangerA MAM | lld:pubmed |
| pubmed-article:8921434 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8921434 | pubmed:volume | 8 | lld:pubmed |
| pubmed-article:8921434 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8921434 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8921434 | pubmed:pagination | 1549-60 | lld:pubmed |
| pubmed-article:8921434 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:8921434 | pubmed:year | 1996 | lld:pubmed |
| pubmed-article:8921434 | pubmed:articleTitle | B7-2 (CD86) is essential for the development of IL-4-producing T cells. | lld:pubmed |
| pubmed-article:8921434 | pubmed:affiliation | Department of Cancer Biology, Harvard School of Public Health, Boston, MA 02115, USA. | lld:pubmed |
| pubmed-article:8921434 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8921434 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
| pubmed-article:8921434 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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