T cell costimulatory receptor CD28 is a primary target for PD-1–mediated inhibition
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Abstract
Immunotherapeutic PD-1–targeted therapies require CD28 to promote cancer cell killing.
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Ligation of PD-1 with its ligands PD-L1 or PD-L2 induces tyrosine phosphorylation of the PD-1 cytoplasmic domain by phosphorylating kinase Lck and subsequent recruitment of cytosolic tyrosine phosphatase SHP-2 and PD-1-associated SHP-2 preferentially dephosphorylates CD28 and suppresses CD28 costimulatory signaling leading to restrained effector T cell function.
“Ligation of PD-1 with its ligands programmed death-ligand 1 or 2 (PD-L1 or PD-L2) induces tyrosine phosphorylation of the PD-1 cytoplasmic domain by phosphorylating kinase Lck and subsequent recruitment of cytosolic tyrosine phosphatase SHP-2 and PD-1-associated SHP-2 preferentially dephosphorylates CD28 and suppresses CD28 costimulatory signaling leading to restrained effector T cell function (49”
From mRNA vaccine with unmodified uridine induces robust type I interferon-dependent anti-tumor immunity in a melanoma model (2022) · cites this paper as [49]
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Experimental — accuracy not yet measuredOvercoming checkpoints through therapeutic antibodies targeting CTLA-4, PD-1, or PD-L1 promotes anti-tumor T cell responses in mice and cancer patients.
“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 Hui et al., 2017
The paper reports that antibodies blocking the PD-L1–PD-1 axis have shown durable clinical benefit in cancer patients, and it discusses studies in which anti–PD-L1/PD-1 therapy restored antitumor T cell responses (passages indexed under Abstract; page unavailable). It does not report that CTLA-4-targeting antibodies promote such responses, or explicitly identify mice as the population in the antitumor-therapy passage. (LLM, conf=0.86)
Experimental — accuracy not yet measuredSHP2 has effects on parallel pathways (e.g., JAK/STAT signaling) and is implicated as an effector of inhibitory signaling by PD-1 and some other immune checkpoint receptors.
“SHP2 also has effects on parallel pathways (e.g., JAK/STAT signaling) and is implicated as an effector of inhibitory signaling by PD-1 and some other immune checkpoint receptors (Hui et al., 2017; Peled et al., 2018; Yokosuka et al., 2012).”
From SHP2 inhibition diminishes KRASG12C cycling and promotes tumor microenvironment remodeling (2021) · cites this paper as Hui et al., 2017
CD28 has recently been found to be the primary target of PD-1-mediated dephosphorylation.
“Among these, CD28 has recently been found to be the primary target (45).”
From Anti-PD-1 and Anti-CTLA-4 Therapies in Cancer: Mechanisms of Action, Efficacy, and Limitations (2018) · cites this paper as [45]
The need for both T cell co-stimulation and IL-12 for maximal IFN-γ response likely reflects a requirement for CD28 to rescue exhausted CD8+ T cells and possibly PD-1 limiting CD28 co-stimulation.
“The requirement for both T cell co-stimulation and IL-12 to achieve maximal IFN-γ response likely reflected the need of CD28 to rescue exhausted CD8+ T cells, and possibly also the role of PD-1 in limiting CD28-mediated co-stimulation (Kamphorst et al., 2017; Hui et al., 2017).”
From Successful Anti-PD-1 Cancer Immunotherapy Requires T Cell-Dendritic Cell Crosstalk Involving the Cytokines IFN-γ and IL-12 (2018) · cites this paper as Hui et al., 2017
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- Authors
- Hui, E., Cheung, J., Zhu, J., Su, X., Taylor, M. J., Wallweber, H. A., Sasmal, D. K., Huang, J., Kim, J. M., Mellman, I., & Vale, R. D.
- Affiliations
- Howard Hughes Medical Institute (US)
- Genentech (US)
- University of Chicago (US)
- Corresponding author
- Mellman, Ira
- Vale, Ronald D.
- ORCID
- Venue
- Science
- Published
- 2017-03-31
- Volume
- 355
- Issue
- 6332
- Pages
- 1428-1433
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC6286077
- OpenAlex
- W2592133876
- Cited by
- 1,689
- References
- 68
- Citations by year
- 2026: 121 · 2025: 158 · 2024: 201 · 2023: 203 · 2022: 193 · 2021: 218 · 2020: 224 · 2019: 159 · 2018: 143 · 2017: 63 · 2016: 1 · 2015: 1 · 2012: 1
- FWCI
- 70.99
- Type
- journal article
- Language
- en
- Open access
- green
- doi.org
- Locations
- Science (publishedVersion)
- bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- MPG.PuRe (Max Planck Society) (submittedVersion, other-oa)
- Funders
- Chicago Biomedical Consortium
- NIH (R21AI120010, R00AI106941)
- Topics
- Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Tyrosine Phosphatases
- Keywords
- PD-1, CD28, PD-L1, T cell costimulation, T cell receptor signaling, SHP2, receptor dephosphorylation, T cell activation, anti-PD-1 therapy, cancer immunotherapy
- MeSH terms
- Animals, Humans, Immunotherapy, Lymphocyte Activation, Mice, Inbred C57BL, Neoplasms, Phosphorylation, T-Lymphocytes, CD28 Antigens, Jurkat Cells, Mice, B7-H1 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.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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