Absence of B7-dependent responses in CD28-deficient mice

Jonathan M. Green*, Patricia J. Noel, Anne I. Sperling, Theresa L. Walunas, Gary S. Gray, Jeffrey A. Bluestone, Craig B. Thompson

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

345 Scopus citations

Abstract

Costimulation of T cell proliferation can occur through the CD28 signal transduction pathway. In addition, other cell surface receptors, including the CD28 homolog CTLA-4, have been proposed to be capable of providing costimulatory signals. We have examined the response of CD28-deficient T cells to activation by a variety of agonists. We demonstrate that proliferation of CD28-deficient T cells in the presence of antigen-presenting cells or B7-1 transfectants is markedly reduced. Although CTLA-4 can be expressed on CD28-deficient T cells, we observed no B7-dependent costimulation in the absence of CD28. This data demonstrates that CD28 is the major B7-binding costimulatory ligand on T cells. Furthermore, our data suggest that CD28 is the primary, and perhaps exclusive, costimulatory receptor used by traditional antigen-presenting cells to augment the proliferation of antigenactivated T cells.

Original languageEnglish (US)
Pages (from-to)501-508
Number of pages8
JournalImmunity
Volume1
Issue number6
DOIs
StatePublished - Sep 1994

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Infectious Diseases

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