Costimulation of antitumor immunity by the B7 counterreceptor for the T lymphocyte molecules CD28 and CTLA-4

Lieping Chen, Stephanie Ashe, William A. Brady, Ingegerd Hellström, Karl Erik Hellström, Jeffrey A. Ledbetter, Patrick McGowan, Peter S. Linsley

Research output: Contribution to journalArticle

Abstract

Interaction of the B7 molecule on antigen-presenting cells with its receptors CD28 and CTLA-4 on T cells provides costimulatory signals for T cell activation. We have studied the effects of B7 on antitumor immunity to a murine melanoma that expresses a rejection antigen associated with the E7 gene product of human papillomavirus 16. While this E7+ tumor grows progressively in immunocompetent hosts, cotransfection of its cells with B7 led to tumor regression by a B7-dependent immune response mediated by CD8+ cytolytic T lymphocytes. The immune response induced by E7+B7+ tumor cells also caused regression of E7+ B7- tumors at distant sites and was curative for established E7+B7- micrometastases. Our findings suggest that increasing T cell costimulation through the CD28 and CTLA-4 receptors may have therapeutic usefulness for generating immunity against tumors expressing viral antigens.

Original languageEnglish (US)
Pages (from-to)1093-1102
Number of pages10
JournalCell
Volume71
Issue number7
DOIs
Publication statusPublished - Dec 24 1992
Externally publishedYes

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ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Cell Biology
  • Molecular Biology

Cite this

Chen, L., Ashe, S., Brady, W. A., Hellström, I., Hellström, K. E., Ledbetter, J. A., ... Linsley, P. S. (1992). Costimulation of antitumor immunity by the B7 counterreceptor for the T lymphocyte molecules CD28 and CTLA-4. Cell, 71(7), 1093-1102. https://doi.org/10.1016/S0092-8674(05)80059-5