B7-H1 signaling is integrated during CD8+ T cell priming and restrains effector differentiation

Rachel M. Gibbons, Xin Liu, Susan M. Harrington, Christopher J. Krco, Eugene D. Kwon, Haidong Dong

Research output: Contribution to journalArticlepeer-review

9 Scopus citations


A promising strategy in tumor immunotherapy is the use of activated dendritic cells as vehicles for tumor vaccines with the goal of activating anti-tumor T cell responses. Current formulations for dendritic cell-based immunotherapies have limited effects on patient survival, providing motivation for further investigation of ways to enhance dendritic cell priming of anti-tumor T cell responses. Using a brief in vitro priming model, we have found that B7-H1 expressed by activated dendritic cells is integrated during priming of naïve CD8+ T cells and functions to limit the differentiation of effector T cell responses. CD8+ T cells primed by B7-H1-deficient dendritic cells exhibit increased production of IFN-γ, enhanced target cell killing, and improved anti-tumor activity. Additionally, enhanced memory populations arise from CD8+ T cells primed by B7-H1-deficient dendritic cells. Based on these findings, we suggest that early blockade of B7-H1 signaling should be investigated as a strategy to improve dendritic cell-based anti-tumor immunotherapy.

Original languageEnglish (US)
Pages (from-to)859-867
Number of pages9
JournalCancer Immunology, Immunotherapy
Issue number8
StatePublished - Aug 2014


  • Co-stimulatory signaling
  • T cell priming

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Oncology
  • Cancer Research

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