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
StatePublished - Dec 24 1992
Externally publishedYes

ASJC Scopus subject areas

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

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    Chen, L., Ashe, S., Brady, W. A., Hellström, I., Hellström, K. E., Ledbetter, J. A., McGowan, P., & 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