Adaptive resistance: A tumor strategy to evade immune attack

Authors

  • Sheng Yao,

    1. Department of Immunobiology and Yale Comprehensive Cancer Center, Yale University School of Medicine, New Haven, USA
    2. Amplimmune, INC., Gaithersburg, USA
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  • Lieping Chen

    Corresponding author
    • Department of Immunobiology and Yale Comprehensive Cancer Center, Yale University School of Medicine, New Haven, USA
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Full correspondence: Dr. Lieping Chen, Department of Immunobiology, Yale University School of Medicine, 300 George Street, New Haven, CT 06519, USA.

Fax: +1-410-5020961

e-mail: Lieping.chen@yale.edu

See accompanying article by Dolen and Esendagli

Abstract

A dilemma in cancer immunology is that, although patients often develop active antitumor immune responses, the tumor still outgrows. It has become clear that under the pressure of the host's immune system, cancer cells have adapted elaborate tactics to reduce their immunogenicity (also known as immunoselection) and/or to actively suppress immune cells and promote immune tolerance (also known as immunosubversion). In this issue of the European Journal of Immunology, Dolen and Esendagli [Eur. J. Immunol. 2013. 43: 747–757] show that acute myeloid leukemia (AML) cells develop an adaptive immune phenotype switching mechanism: In response to attack by activated T cells, the leukemia cells quickly downregulate the T-cell costimulatory ligand B7-H2 and reciprocally upregulate the coinhibitory ligands B7-H1 and B7-DC in order to shut down T-cell activation via the PD-1 pathway. These novel findings and their relevance for cancer immunotherapy, especially potential applications in PD-1 check-point blockade therapy are discussed in this Commentary.

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