Cited by 967Cancer Immunotherapy and BiomarkersT-cell and B-cell ImmunologyImmunotherapy and Immune Responses

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Blockade of CTLA-4 on both effector and regulatory T cell compartments contributes to the antitumor activity of anti-CTLA-4 antibodies

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Peggs, Karl S., Quezada, Sergio A., Chambers, Cynthia A., Korman, Alan J., Allison, James P.·2009·Journal of Experimental Medicine

DOI 10.1084/jem.20082492PMC PMC2722174

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Abstract

Cytotoxic T lymphocyte–associated antigen 4 (CTLA-4) is a critical negative regulator of immune responses. Uniquely among known inhibitory receptors, its genetic ablation results in a fulminating and fatal lymphoproliferative disorder. This central regulatory role led to the development of antibodies designed to block CTLA-4 activity in vivo, aiming to enhance immune responses against cancer. Despite their preclinical efficacy and promising clinical activity against late stage metastatic melanoma, the critical cellular targets for their activity remains unclear. In particular, debate has focused on whether the effector T cell (Teff) or regulatory T cell (T reg cell) compartment is the primary target of antibody-mediated blockade. We developed a mouse expressing human instead of mouse CTLA-4, allowing us to evaluate the independent contributions of CTLA-4 blockade of each T cell compartment during cancer immunotherapy in an in vivo model of mouse melanoma. The data show that although blockade on effector cells significantly improves tumor protection, unicompartmental blockade on regulatory cells completely fails to enhance antitumor responses. However, concomitant blockade of both compartments leads to a synergistic effect and maximal antitumor activity. We conclude that the combination of direct enhancement of Teff cell function and concomitant inhibition of T reg cell activity through blockade of CTLA-4 on both cell types is essential for mediating the full therapeutic effects of anti–CTLA-4 antibodies during cancer immunotherapy.

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Authors: Peggs, K. S., Quezada, S. A., Chambers, C. A., Korman, A. J., & Allison, J. P.
Affiliations: Memorial Sloan Kettering Cancer Center (US)
University of Massachusetts Chan Medical School (US)
Medarex, Inc., Milpitas, CA 95035 3
Corresponding author: Allison, James P.
ORCID: Peggs, Karl S.
Quezada, Sergio A.
Korman, Alan J.
Allison, James P.
Venue: Journal of Experimental Medicine
Publisher: Rockefeller University Press
Published: 2009-07-06
Volume: 206
Issue: 8
Pages: 1717-1725
ISSN: 0022-1007 (ISSN-L)
1540-9538
DOI: 10.1084/jem.20082492
PMC: PMC2722174
OpenAlex: W2013043293
Cited by: 967
References: 34
Citations by year: 2026: 17 · 2025: 46 · 2024: 57 · 2023: 56 · 2022: 51 · 2021: 54 · 2020: 59 · 2019: 64 · 2018: 78 · 2017: 82 · 2016: 78 · 2015: 81 · 2014: 56 · 2013: 60 · 2012: 39
FWCI: 20.80
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: The Journal of Experimental Medicine (publishedVersion)
PubMed Central (publishedVersion, cc-by-nc-sa)
PubMed (publishedVersion)
UCL Discovery (University College London) (submittedVersion)
Funders: Howard Hughes Medical Institute
Cancer Research Institute
Bristol-Myers Squibb
Memorial Sloan-Kettering Cancer Center
University College London
Topics: Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
Keywords: CTLA-4, anti-CTLA-4 antibody, regulatory T cells, effector T cells, cancer immunotherapy, melanoma, immune checkpoint blockade, humanized mice, antitumor immunity, T cell tolerance
MeSH terms: Animals, Antibodies, Neoplasm, Humans, Immunosuppression Therapy, Immunotherapy, Melanoma, Experimental, Mice, Inbred C57BL, Mice, Transgenic, Recombinant Proteins, Antigens, CD, T-Lymphocyte Subsets, Mice, Knockout, Cell Line, Tumor, T-Lymphocytes, Regulatory, Mice, CTLA-4 Antigen, In Vitro Techniques

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Blockade of CTLA-4 on both effector and regulatory T cell compartments contributes to the antitumor activity of anti-CTLA-4 antibodies

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