Cited by 5,025Cancer Immunotherapy and BiomarkersImmunotherapy and Immune ResponsesT-cell and B-cell Immunology

Tumor-associated B7-H1 promotes T-cell apoptosis: A potential mechanism of immune evasion

Dong, Haidong, Strome, Scott E., Salomao, Diva R., Tamura, Hideto, Hirano, Fumiya, Flies, Dallas B., Roche, Patrick C., Lu, Jun +5 more·2002·Nature Medicine

Abstract

B7-H1, a recently described member of the B7 family of costimulatory molecules, is thought to be involved in the regulation of cellular and humoral immune responses through the PD-1 receptor on activated T and B cells. We report here that, except for cells of the macrophage lineage, normal human tissues do not express B7-H1. In contrast, B7-H1 is abundant in human carcinomas of lung, ovary and colon and in melanomas. The pro-inflammatory cytokine interferon-gamma upregulates B7-H1 on the surface of tumor cell lines. Cancer cell-associated B7-H1 increases apoptosis of antigen-specific human T-cell clones in vitro, and the apoptotic effect of B7-H1 is mediated largely by one or more receptors other than PD-1. In addition, expression of B7-H1 on mouse P815 tumor increases apoptosis of activated tumor-reactive T cells and promotes the growth of highly immunogenic B7-1(+) tumors in vivo. These findings have implications for the design of T cell-based cancer immunotherapy.

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Crossref · 10.1038/nm730

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Authors
Dong, H., Strome, S. E., Salomao, D. R., Tamura, H., Hirano, F., Flies, D. B., Roche, P. C., Lu, J., Zhu, G., Tamada, K., Lennon, V. A., Celis, E., & Chen, L.
Affiliations
Mayo Clinic (US)
Corresponding author
Chen, Lieping
Venue
Nature Medicine
Published
2002-06-24
Volume
8
Issue
8
Pages
793-800
ISSN
  • 1078-8956 (ISSN-L)
  • 1546-170X
OpenAlex
W2016983859
Cited by
5,025
References
39
Citations by year
2026: 162 · 2025: 222 · 2024: 250 · 2023: 298 · 2022: 296 · 2021: 367 · 2020: 377 · 2019: 388 · 2018: 424 · 2017: 406 · 2016: 364 · 2015: 316 · 2014: 175 · 2013: 178 · 2012: 106
FWCI
24.42
Type
journal article
Language
en
Open access
closed
Locations
  • Nature Medicine (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Cancer Institute (R01CA037343, CA-85721, CA79915, CA82677, CA-37343, R01CA079915, R01CA080782, CA80782, R01CA082677, R01CA085721, CA 15083, P30CA015083)
Topics
  • Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
  • Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
Keywords
PD-L1, T cell apoptosis, immune evasion, PD-1 receptor, interferon-gamma, costimulatory molecules, tumor immunogenicity, melanoma, lung cancer, ovarian carcinoma, colon cancer
MeSH terms
Animals, Antibodies, Monoclonal, Antigens, Surface, Antineoplastic Agents, Blood Proteins, Cell Separation, Female, Flow Cytometry, Humans, Lymphocyte Activation, Melanoma, Membrane Glycoproteins, Mice, Inbred Strains, Neoplasms, Peptides, Recombinant Fusion Proteins, T-Lymphocytes, Cytotoxic, Tumor Cells, Cultured, Tumor Necrosis Factor-alpha, Signal Transduction, Antigens, CD, Apoptosis, B7-1 Antigen, Tumor Escape, Apoptosis Regulatory Proteins, Mice, TNF-Related Apoptosis-Inducing Ligand, Fas Ligand Protein, B7-H1 Antigen, Programmed Cell Death 1 Receptor

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