Blockade of PD‐L1 (B7‐H1) augments human tumor‐specific T cell responses in vitro
Open accessAbstract
Human tumors frequently escape immune destruction, despite the presence of cyototoxic T cells (CTL) recognizing tumor‐associated antigens (TAA). We have previously shown that programmed death ligand‐1 (PD‐L1), a recently identified ligand of the B7 superfamily, is expressed on murine tumors and can inhibit antitumor immune responses. To evaluate the clinical relevance of our animal model findings, we examined human tumors and tumor‐specific T cells. We found PD‐L1 to be constitutively expressed on human renal cell carcinoma (RCC) cell lines and upregulated on human melanoma cell lines upon exposure to interferon‐gamma. Similarly, we found binding of anti‐PD‐L1 monoclonal antibody (mAb) on frozen sections from RCC and melanomas, but not on normal tissues. The corresponding inhibitory receptor of PD‐L1, PD‐1, revealed a higher expression on tumor‐infiltrating lymphocytes than on peripheral blood lymphocytes (PBL) from melanoma patients upon specific antigen stimulation. Stimulation of PBL from healthy donors with peptide‐loaded dendritic cells in the presence of anti‐PD‐L1 mAb altered neither the total T cell numbers after expansion, nor the percentage of peptide‐specific CTL, when providing a T cell help by addition of cytokines. However, when stimulating TAA‐specific CTL and T helper cells with Ag‐pulsed dendritic cells in the absence of exogenous cytokines, PD‐L1 blockade increased the cytokine production. Similar to the data achieved in the murine system, the blockade of PD‐L1 on human tumors resulted in enhanced cytolytic activity of TAA‐specific CTLs and cytokine production of TAA‐specific T helper cells when interacting directly with the tumor. In summary, our data suggest that PD‐L1/PD‐1 interactions negatively regulate T cell effector functions predominately in the absence of exogenous cytokine support, indicating an important role for this pathway in tumor evasion. © 2006 Wiley‐Liss, Inc.
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In animal models, introducing B7-1 into tumors or blocking inhibitory B7 family members reduces tumor growth or causes spontaneous tumor rejection.
“Animal model studies have shown that introduction of B7-1 into tumors by transfection or blockade of inhibitory B7 family members can reduce tumor growth or result in spontaneous tumor rejection in vivo [7–13].”
From T cell anergy, exhaustion, senescence, and stemness in the tumor microenvironment (2013) · cites this paper as [13]
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- Authors
- Blank, C., Kuball, J., Voelkl, S., Wiendl, H., Becker, B., Walter, B., Majdic, O., Gajewski, T. F., Theobald, M., Andreesen, R., & Mackensen, A.
- Affiliations
- University of Regensburg (DE)
- University of Würzburg (DE)
- University of Vienna (AT)
- University of Chicago (US)
- Johannes Gutenberg University Mainz (DE)
- Corresponding author
- Blank, Christian
- Venue
- International Journal of Cancer
- Publisher
- Wiley
- Published
- 2006-04-27
- Volume
- 119
- Issue
- 2
- Pages
- 317-327
- ISSN
- 0020-7136 (ISSN-L)
- 1097-0215
- OpenAlex
- W2039427849
- Cited by
- 297
- References
- 81
- Citations by year
- 2026: 3 · 2025: 7 · 2024: 8 · 2023: 10 · 2022: 10 · 2021: 15 · 2020: 7 · 2019: 12 · 2018: 13 · 2017: 23 · 2016: 21 · 2015: 21 · 2014: 22 · 2013: 21 · 2012: 19
- FWCI
- 9.19
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- International Journal of Cancer (publishedVersion)
- PubMed (publishedVersion)
- University of Regensburg Publication Server (University of Regensburg) (acceptedVersion)
- University of Regensburg Publication Server (University of Regensburg)
- Funders
- Deutsche Forschungsgemeinschaft (SFB 432)
- José Carreras Leukämie-Stiftung
- Deutsche Krebshilfe
- 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, PD-1, immune checkpoint blockade, tumor-specific T cell responses, cytotoxic T lymphocytes, tumor-associated antigens, renal cell carcinoma, melanoma, interferon-gamma, tumor-infiltrating lymphocytes, dendritic cell activation, cytokine production, tumor immune evasion, anti-PD-L1 monoclonal antibody
- MeSH terms
- Antibodies, Monoclonal, Antigens, Differentiation, Antineoplastic Agents, Carcinoma, Renal Cell, Flow Cytometry, Humans, Immunohistochemistry, Kidney Neoplasms, Melanoma, T-Lymphocytes, Cytotoxic, Tumor Cells, Cultured, Antigens, CD, Up-Regulation, Gene Expression Regulation, Neoplastic, B7-1 Antigen, B7-H1 Antigen, CTLA-4 Antigen
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