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The B7 Family and Cancer Therapy: Costimulation and Coinhibition

Xingxing Zang and James P. Allison
Xingxing Zang
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James P. Allison
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DOI: 10.1158/1078-0432.CCR-07-1030 Published September 2007
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Abstract

The activation and development of an adaptive immune response is initiated by the engagement of a T-cell antigen receptor by an antigenic peptide-MHC complex. The outcome of this engagement is determined by both positive and negative signals, costimulation and coinhibition, generated mainly by the interaction between the B7 family and their receptor CD28 family. The importance of costimulation and coinhibition of T cells in controlling immune responses is exploited by tumors as immune evasion pathways. Absence of the expression of costimulatory B7 molecules renders tumors invisible to the immune system, whereas enhanced expression of inhibitory B7 molecules protects them from effective T cell destruction. Therefore, the manipulation of these pathways is crucial for developing effective tumor immunotherapy. Translation of our basic knowledge of costimulation and coinhibition into early clinical trials has shown considerable promise.

  • T-cell
  • costimulation
  • coinhibition
  • cancer therapy

Footnotes

  • Grant support: Howard Hughes Medical Institute and the NIH.

  • Received April 30, 2007.
  • Revision received June 11, 2007.
  • Accepted June 27, 2007.
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Clinical Cancer Research: 13 (18)
September 2007
Volume 13, Issue 18
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The B7 Family and Cancer Therapy: Costimulation and Coinhibition
Xingxing Zang and James P. Allison
Clin Cancer Res September 15 2007 (13) (18) 5271-5279; DOI: 10.1158/1078-0432.CCR-07-1030

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The B7 Family and Cancer Therapy: Costimulation and Coinhibition
Xingxing Zang and James P. Allison
Clin Cancer Res September 15 2007 (13) (18) 5271-5279; DOI: 10.1158/1078-0432.CCR-07-1030
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  • Article
    • Abstract
    • Extended B7 Family and CD28 Family
    • Enhancement of Costimulation: B7-1, B7-2, B7h–Transfected Tumor Cell Vaccines
    • Blockade of Coinhibition: Anti–CTLA-4 Therapy
    • PD-L1/PD-1: Tumor Evasion Pathway
    • Tumor-Associated B7-H3 and B7x: Last-ditch Mechanism
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Clinical Cancer Research
eISSN: 1557-3265
ISSN: 1078-0432

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