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The blockade of immune checkpoints in cancer immunotherapy
Open accessAbstract
Among the most promising approaches to activating therapeutic antitumour immunity is the blockade of immune checkpoints. Immune checkpoints refer to a plethora of inhibitory pathways hardwired into the immune system that are crucial for maintaining self-tolerance and modulating the duration and amplitude of physiological immune responses in peripheral tissues in order to minimize collateral tissue damage. It is now clear that tumours co-opt certain immune-checkpoint pathways as a major mechanism of immune resistance, particularly against T cells that are specific for tumour antigens. Because many of the immune checkpoints are initiated by ligand-receptor interactions, they can be readily blocked by antibodies or modulated by recombinant forms of ligands or receptors. Cytotoxic T-lymphocyte-associated antigen 4 (CTLA4) antibodies were the first of this class of immunotherapeutics to achieve US Food and Drug Administration (FDA) approval. Preliminary clinical findings with blockers of additional immune-checkpoint proteins, such as programmed cell death protein 1 (PD1), indicate broad and diverse opportunities to enhance antitumour immunity with the potential to produce durable clinical responses.
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“Recently, immunotherapies have shown promising results for reducing metastasis in melanoma or kidney cancer patients[1, 2].”
From Microfluidics: A New Tool for Modeling Cancer–Immune Interactions (2016) · cites this paper as [2]
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“Under normal physiological conditions, inhibitory immune checkpoint molecules are essential to maintain self-tolerance and prevent autoimmunity [1,2]”
From Characterizing the molecular regulation of inhibitory immune checkpoints with multimodal single-cell screens (2021) · cites this paper as [2]
In the citing paper
“there was strong down-regulation of several proteins with potential roles in modifying the response to immunotherapies exclusively in co-culture conditions, including CXCR4 (CD184), c-KIT (CD117) and KDR (CD309)23,24”
From Multimodal pooled Perturb-CITE-seq screens in patient models define mechanisms of cancer immune evasion (2021) · cites this paper as [23]
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“There is an active imbalance between stimulatory and inhibitory B7 family members in the tumor microenvironment [1,3,7,8].”
From T cell anergy, exhaustion, senescence, and stemness in the tumor microenvironment (2013) · cites this paper as [3]
In the citing paper
“Furthermore, TGF-β signaling in T cells activates SHP1 expression, which represses protein tyrosine kinase activities required for TCR signaling203,204.”
From TGFβ biology in cancer progression and immunotherapy (2021) · cites this paper as [204]
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“In monotherapy, checkpoint inhibitors have resulted in impressive effects and durable responses in patients with highly refractory and late-stage cancers, such as metastatic melanoma and non-small cell lung cancer (NSCLC) [216].”
From Three decades of messenger RNA vaccine development (2019) · cites this paper as [216]
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Flagged first, then by citations
1 of the 129 references couldn’t be matched to a known paper.
Research works printed but not linked: 1
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Cited by
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PD-1 and PD-L1 Immune Checkpoint Blockade to Treat Breast Cancer
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“All patients All doses 49 5 10 (3-22) 6 12 (5-25) 31 (17-45)”
InfluentialSelf-citationCancer immunotherapy using checkpoint blockade
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Metadata
- Authors
- Pardoll, D. M.
- Affiliations
- Johns Hopkins University (US)
- Corresponding author
- Pardoll, Drew M.
- ORCID
- Pardoll, Drew M.
- Venue
- Nature Reviews Cancer
- Published
- 2012-03-22
- Volume
- 12
- Issue
- 4
- Pages
- 252-264
- ISSN
- 1474-175X (ISSN-L)
- 1474-1768
- PMC
- PMC4856023
- OpenAlex
- W2066671159
- Cited by
- 13,838
- References
- 129
- Citations by year
- 2026: 652 · 2025: 910 · 2024: 1153 · 2023: 1202 · 2022: 1302 · 2021: 1456 · 2020: 1409 · 2019: 1236 · 2018: 1197 · 2017: 1146 · 2016: 897 · 2015: 647 · 2014: 339 · 2013: 240 · 2012: 39
- FWCI
- 41.84
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Nature reviews. Cancer (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Melanoma Research Alliance
- Hussman Foundation
- National Cancer Institute (P30CA021765, P30CA006973)
- 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
- immune checkpoint, cancer immunotherapy, immune checkpoint blockade, CTLA-4, PD-1, tumor immune evasion, antitumor immunity, self-tolerance, ligand-receptor interactions, antibody therapy, combination therapy, immune resistance
- MeSH terms
- Animals, Antigens, Neoplasm, Clinical Trials as Topic, Humans, Immunotherapy, Neoplasms, Tumor Escape, Cancer Vaccines, Molecular Targeted Therapy, CTLA-4 Antigen, Programmed Cell Death 1 Receptor
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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