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Enhancement of Antitumor Immunity by CTLA-4 Blockade
Abstract
One reason for the poor immunogenicity of many tumors may be that they cannot provide signals for CD28-mediated costimulation necessary to fully activate T cells. It has recently become apparent that CTLA-4, a second counterreceptor for the B7 family of costimulatory molecules, is a negative regulator of T cell activation. Here, in vivo administration of antibodies to CTLA-4 resulted in the rejection of tumors, including preestablished tumors. Furthermore, this rejection resulted in immunity to a secondary exposure to tumor cells. These results suggest that blockade of the inhibitory effects of CTLA-4 can allow for, and potentiate, effective immune responses against tumor cells.
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In the citing paper
“Overcoming such checkpoints through the use of therapeutic antibodies targeting the CTLA-4, PD-1, or PD-L1 cell-surface receptors was shown to be instrumental in promoting anti-tumor T cell responses in mice and in cancer patients”
From LXR/ApoE Activation Restricts Innate Immune Suppression in Cancer (2018) · cites this paper as Leach et al., 1996
In the citing paper
“Additionally, studies by Allison et al. using murine colon carcinoma and fibrosarcoma models demonstrated that co-administration of anti-CTLA-4 antibodies with tumor lysate-loaded dendritic cells can reduce Tregs, increase CD8+ lymphocytes, inhibit metastatic growth, and prolong survival [121].”
From Current and Future Trends of Colorectal Cancer Treatment: Exploring Advances in Immunotherapy (2024) · cites this paper as [121]
In the citing paper
“CTLA-4, another inhibitory receptor that is expressed on CD4+ Treg and activated CD8+ T cells, restrains costimulation of T cells and thus also serves as immune checkpoint357,358.”
From TGFβ biology in cancer progression and immunotherapy (2021) · cites this paper as [358]
In the citing paper
“Immune checkpoint therapy (ICT) can provide durable clinical responses and improve overall survival.”
From The Next Decade of Immune Checkpoint Therapy (2021) · cites this paper as [1]
In the citing paper
“In early studies, an anti-CTLA4 antibody prevented CTLA4 from engaging B7, leading to prolonged T-cell responses and eradication of cancer cells (1).”
From The Next Decade of Immune Checkpoint Therapy (2021) · cites this paper as [1]
In the citing paper
“Similarly, the in vivo administration of anti-CTLA4 antibodies enhanced the antitumor effect of tumor-infiltrating T cells, leading to regression of established tumors and long-lived immunity in tumor models (1).”
From The Next Decade of Immune Checkpoint Therapy (2021) · cites this paper as [1]
In the citing paper
“Initial preclinical studies demonstrated that blockade of CTLA-4 with an antibody led to an enhanced and a long-lasting anti-tumor immune response and regression of immunogenic tumors (Leach et al., 1996; van Elsas et al., 1999).”
From Hallmarks of response, resistance, and toxicity to immune checkpoint blockade (2021) · cites this paper as Leach et al., 1996
In the citing paper
“CTLA-4 blockade did not demonstrate substantial autoimmunity (Leach et al., 1996; Rowshanravan et al., 2018).”
From Hallmarks of response, resistance, and toxicity to immune checkpoint blockade (2021) · cites this paper as Leach et al., 1996
In the citing paper
“ICB treatment in pre-clinical models did not lead to overwhelming autoimmune pathology”
From Hallmarks of response, resistance, and toxicity to immune checkpoint blockade (2021) · cites this paper as Leach et al., 1996
Citations
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Metadata
- Authors
- Leach, D. R., Krummel, M. F., & Allison, J. P.
- Affiliations
- University of California, Berkeley (US)
- Corresponding author
- Allison, James P.
- Venue
- Science
- Published
- 1996-03-22
- Volume
- 271
- Issue
- 5256
- Pages
- 1734-1736
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W2094366129
- Cited by
- 3,955
- References
- 4
- Citations by year
- 2026: 114 · 2025: 210 · 2024: 248 · 2023: 271 · 2022: 254 · 2021: 327 · 2020: 331 · 2019: 317 · 2018: 243 · 2017: 216 · 2016: 204 · 2015: 188 · 2014: 88 · 2013: 113 · 2012: 87
- FWCI
- 20.64
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Cancer Institute (CA40041, CA 09179, R01CA057986, T32CA009179, CA57986)
- 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
- CTLA-4, CTLA-4 blockade, antitumor immunity, tumor immunogenicity, CD28 costimulation, B7 costimulatory molecules, T cell activation, tumor rejection, anti-CTLA-4 antibody
- MeSH terms
- Abatacept, Animals, Antibodies, Antigens, Differentiation, Female, Graft Rejection, Immunologic Memory, Lymphocyte Activation, Mice, Inbred A, Mice, Inbred BALB C, Neoplasm Transplantation, Neoplasms, Experimental, T-Lymphocytes, Transfection, Tumor Cells, Cultured, Antigens, CD, CD28 Antigens, B7-1 Antigen, Immunoconjugates, Mice, CTLA-4 Antigen
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