B7-H1 expressed by activated CD8 T cells is essential for their survival

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

Research output: Contribution to journalArticlepeer-review

43 Scopus citations

Abstract

An immunoinhibitory role of B7 homologue 1 (B7-H1) expressed by non-T cells has been established; however, the function of B7-H1 expressed by T cells is not clear. Peak expression of B7-H1 on Ag-primed CD8 T cells was observed during the contraction phase of an immune response. Unexpectedly, B7-H1 blockade at this stage reduced the numbers of effector CD8 T cells, suggesting B7-H1 blocking Ab may disturb an unknown function of B7-H1 expressed by CD8 T cells. To exclusively examine the role of B7-H1 expressed by T cells, we introduced B7-H1 deficiency into TCR transgenic (OT-1) mice. Naive B7-H1-deficient CD8 T cells proliferated normally following Ag stimulation; however, once activated, they underwent more robust contraction in vivo and more apoptosis in vitro. In addition, B7-H1-deficient CD8 T cells were more sensitive to Ca-dependent and Fas ligand-dependent killing by cytotoxic T lymphocytes. Activation-induced Bcl-xL expression was lower in activated B7-H1-deficient CD8 T cells, whereas Bcl-2 and Bim expression were comparable to the wild type. Transfer of effector B7-H1-deficient CD8 T cells failed to suppress tumor growth in vivo. Thus, upregulation of B7-H1 on primed T cells helps effector T cells survive the contraction phase and consequently generate optimal protective immunity.

Original languageEnglish (US)
Pages (from-to)5606-5614
Number of pages9
JournalJournal of Immunology
Volume187
Issue number11
DOIs
StatePublished - Dec 1 2011

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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