Cancer Immunology, Immunotherapy

, Volume 56, Issue 5, pp 739–745

Contribution of the PD-L1/PD-1 pathway to T-cell exhaustion: an update on implications for chronic infections and tumor evasion

Symposium Paper

DOI: 10.1007/s00262-006-0272-1

Cite this article as:
Blank, C. & Mackensen, A. Cancer Immunol Immunother (2007) 56: 739. doi:10.1007/s00262-006-0272-1


Recent clinical data support ideas of Programmed death receptor-ligand 1 (PD-L1; also called B7-H1, CD274) playing an important role in immune evasion of tumor cells. Expression of PD-L1 on tumors strongly correlates with the survival of cancer patients. PD-L1 on tumors interacts with the co-inhibitory molecule Programmed death receptor-1 (PD-1, CD279) on T cells mediating decreased TCR-mediated proliferation and cytokine production. In animal tumor models, blockade of PD-L1/PD-1 interactions resulted in an improved tumor control. In addition, exhausted T cells during chronic viral infections could be revived by PD-L1 blockade. Thus, targeting PD-L1/PD-1 interactions might improve the efficacy of adoptive cell therapies (ACT) of chronic infections as well as cancers. Obstacles for a general blockade of PD-L1 might be its role in mediating peripheral tolerance. This review discusses the currently available data concerning the role of PD-L1 in tumor immune evasion and envisions possibilities for implementation into ACT for cancer patients.

Copyright information

© Springer-Verlag 2006

Authors and Affiliations

  1. 1.Department of Hematology and OncologyUniversity of RegensburgRegensburgGermany