ArticleMolecular therapy : the journal of the American Society of Gene Therapy2012
Long-term persistence of CD4(+) but rapid disappearance of CD8(+) T cells expressing an MHC class I-restricted TCR of nanomolar affinity.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
33 citing papers in PubMed, 46 citations in OpenAlex.
- Evaluating the effects of CD8/CD4 on T cell function in terms of TCR-pMHC-coreceptor catch and slip bonds.Frontiers in immunology · 2026Article
- Evaluating the effects of CD8/CD4 on T cell function in terms of TCR-pMHC-coreceptor catch and slip bonds.bioRxiv : the preprint server for biology · 2025Article
- Natural TCRs targeting KRASG12V display fine specificity and sensitivity to human solid tumors.The Journal of clinical investigation · 2024Article
- CD4Science immunology · 2024Article
- The landscape of T cell antigens for cancer immunotherapy.Nature cancer · 2023Review
- Development of a CD8 co-receptor independent T-cell receptor specific for tumor-associated antigen MAGE-A4 for next generation T-cell-based immunotherapy.Journal for immunotherapy of cancer · 2021Article
- OX40 as a novel target for the reversal of immune escape in colorectal cancer.American journal of translational research · 2021Review
- Chimeric antigen receptor T cell therapy for pediatric and young adult B cell acute lymphoblastic leukemia.Expert review of clinical immunology · 2020Article
- Review
- Chronic TCR-MHC (self)-interactions limit the functional potential of TCR affinity-increased CD8 T lymphocytes.Journal for immunotherapy of cancer · 2019Article
- Improving T Cell Receptor On-Target Specificity via Structure-Guided Design.Molecular therapy : the journal of the American Society of Gene Therapy · 2019Article
- T Cell Receptors for Gene Transfer in Adoptive T Cell Therapy.Critical reviews in immunology · 2019Review
- Article
- Expanding the Therapeutic Window for CAR T Cell Therapy in Solid Tumors: The Knowns and Unknowns of CAR T Cell Biology.Frontiers in immunology · 2018Review
- Combination of radiotherapy and vaccination overcomes checkpoint blockade resistance.Oncotarget · 2016Article
- Eradication of Large Solid Tumors by Gene Therapy with a T-Cell Receptor Targeting a Single Cancer-Specific Point Mutation.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016Article
- Adoptive T Cell Therapies: A Comparison of T Cell Receptors and Chimeric Antigen Receptors.Trends in pharmacological sciences · 2016Review
- Recent advances in T-cell engineering for use in immunotherapy.F1000Research · 2016Review
- New Strategies in Engineering T-cell Receptor Gene-Modified T cells to More Effectively Target Malignancies.Clinical cancer research : an official journal of the American Association for Cancer Research · 2015Review
- Superantigens produced by catheter-associated Staphylococcus aureus elicit systemic inflammatory disease in the absence of bacteremia.Journal of leukocyte biology · 2015Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Most T cells have T cell receptors (TCR) of micromolar affinity for peptide-major histocompatibility complex (MHC) ligands, but genetic engineering can generate TCRs of nanomolar affinity. The affinity of the TCR used, m33, for its cognate non-self peptide-MHC-I complex (SIYRYYGL-K(b)) is 1,000-fold higher than of the wild-type TCR 2C. The affinity of m33 for the self-peptide dEV-8 on K(b) is only twofold higher. Mouse CD8(+) T cells transduced with an m33-encoding retrovirus showed binding of SIY-K(b) and potent function in vitro, but in vivo these T cells disappeared within hours after transfer into syngeneic hosts without causing graft-versus-host disease (GVHD). Accordingly, in cases where such CD8-dependent self-reactivity might occur in human adoptive T cell therapies, our results show that a peripheral T-cell deletion mechanism could operate to avoid reactions with the host. In contrast to CD8(+) T cells, we show that CD4(+) T cells expressing m33 survived for months in vivo. Furthermore, the m33-transduced CD4(+) T cells were able to mediate antigen-specific rejection of 6-day-old tumors. Together, we show that CD8(+) T cell expressing a MHC class I-restricted high-affinity TCR were rapidly deleted whereas CD4(+) T cells expressing the same TCR survived and provided function while being directed against a class I-restricted antigen.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.