Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
1997-2-10
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0953-8178
pubmed:author
pubmed:issnType
Print
pubmed:volume
8
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1549-60
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:8921434-Animals, pubmed-meshheading:8921434-Antibodies, Blocking, pubmed-meshheading:8921434-Antigens, CD, pubmed-meshheading:8921434-Antigens, CD80, pubmed-meshheading:8921434-Antigens, CD86, pubmed-meshheading:8921434-Cell Differentiation, pubmed-meshheading:8921434-Cell Separation, pubmed-meshheading:8921434-Immunoglobulin Fab Fragments, pubmed-meshheading:8921434-Interleukin-4, pubmed-meshheading:8921434-Lymphocyte Activation, pubmed-meshheading:8921434-Membrane Glycoproteins, pubmed-meshheading:8921434-Mice, pubmed-meshheading:8921434-Mice, Inbred BALB C, pubmed-meshheading:8921434-Mice, Transgenic, pubmed-meshheading:8921434-Recombinant Proteins, pubmed-meshheading:8921434-Spleen, pubmed-meshheading:8921434-T-Lymphocytes, pubmed-meshheading:8921434-T-Lymphocytes, Helper-Inducer
pubmed:year
1996
pubmed:articleTitle
B7-2 (CD86) is essential for the development of IL-4-producing T cells.
pubmed:affiliation
Department of Cancer Biology, Harvard School of Public Health, Boston, MA 02115, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't