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PMID: 9820499 Published · ppublish English Journal Article Research Support, U.S. Gov't, P.H.S.

B7.1 is a quantitatively stronger costimulus than B7.2 in the activation of naive CD8+ TCR-transgenic T cells.

Journal of immunology (Baltimore, Md. : 1950) ·Vol. 161 ·No. 10 ·1998-11-15 ·Pages 5268-75

Fields PE, Finch RJ, Gray GS, Zollner R, Thomas JL, Sturmhoefel K, Lee K, Wolf S, Gajewski TF, Fitch FW

Abstract

Using a TCR transgenic mouse bred onto a recombinase-activating gene-2-deficient background, we have examined the influence of B7.1 and B7.2 on activation of naive, CD8+ T cells in vitro. We found that B7.1 was a more potent costimulus than B7.2 for induction of proliferation and IL-2 production by naive CD8+ T cells. This difference appeared to be quantitative in nature, as determined using transfectants expressing various defined levels of B7.1 or B7.2, or using purified B7.1 or B7.2 fusion proteins. In contrast to the quantitative differences seen in stimulation of naive T cells, B7.1 and B7.2 were comparable in their ability to costimulate responses in T cells previously primed in vitro. In addition, primed, but not naive, T cells were capable of proliferating and producing IL-2 in response to a TCR stimulus alone, apparently in the absence of B7 costimulation. Lastly, we found that B7.1 and B7.2 were equivalently capable of driving differentiation of naive CD8+ T cells into an IL-4-producing phenotype when exogenous IL-4 was added to the primary culture or to an IFN-gamma-producing phenotype in the presence of IL-12. These results indicate that signals generated by B7.1 and B7.2 are qualitatively similar, but that B7.1 is quantitatively stronger than B7.2. Further, our results indicate that the activation state of the responding T cell may influence the efficiency with which the T cell can respond to a costimulatory signal provided by either B7.1 or B7.2.

MeSH Terms
Animals Antibodies, Monoclonal/pharmacology Antigens, CD/biosynthesis,genetics,immunology B7-1 Antigen/biosynthesis,genetics,immunology B7-2 Antigen CD3 Complex/immunology CD8-Positive T-Lymphocytes/immunology,metabolism Homeodomain Proteins/genetics Humans Lymphocyte Activation/genetics,immunology Mast-Cell Sarcoma Membrane Glycoproteins/biosynthesis,genetics,immunology Mice Mice, Mutant Strains Mice, Transgenic Receptors, Antigen, T-Cell/genetics Recombinant Fusion Proteins/immunology,pharmacology T-Lymphocyte Subsets/immunology,metabolism Transfection/immunology Tumor Cells, Cultured
Chemicals
Antibodies, Monoclonal Antigens, CD B7-1 Antigen B7-2 Antigen CD3 Complex CD86 protein, human Cd86 protein, mouse Homeodomain Proteins Membrane Glycoproteins Receptors, Antigen, T-Cell Recombinant Fusion Proteins RAG-1 protein
Authors & Affiliations
10 authors, click to expand affiliations / ORCID
Fields P E
Department of Pathology, University of Chicago, IL 60637, USA.
Finch R J
Gray G S
Zollner R
Thomas J L
Sturmhoefel K
Lee K
Wolf S
Gajewski T F
Fitch F W
Article Info
Journal
Journal of immunology (Baltimore, Md. : 1950)
Abbr.
J Immunol
ISSN
0022-1767
Published
1998-11-15
Pages
5268-75
Language
English
Region
United States
NLM ID
2985117R
Subset
IM
Grants
NCI NIH HHS · CA14599 · United States
NIAID NIH HHS · P01AI29531 · United States
NIDDK NIH HHS · P01DK49799 · United States
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