ArticleJournal of immunology (Baltimore, Md. : 1950)2008
The proline-rich sequence of CD3epsilon as an amplifier of low-avidity TCR signaling.
Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed, 55 citations in OpenAlex.
- From TCR fundamental research to innovative chimeric antigen receptor design.Nature reviews. Immunology · 2025Review
- The TCR and LCK: foundations for T-cell activation and therapeutic innovation.Frontiers in immunology · 2025Review
- Mechanism of Action and Pharmacokinetics of Approved Bispecific Antibodies.Biomolecules & therapeutics · 2024Review
- Modulating T Cell Responses by Targeting CD3.Cancers · 2023Review
- T-cell Receptor Is a Threshold Detector: Sub- and Supra-Threshold Stochastic Resonance in TCR-MHC Clusters on the Cell Surface.Entropy (Basel, Switzerland) · 2022Review
- Comparative analysis of TCR and CAR signaling informs CAR designs with superior antigen sensitivity and in vivo function.Science signaling · 2021Article
- Small molecule AX-024 reduces T cell proliferation independently of CD3ϵ/Nck1 interaction, which is governed by a domain swap in the Nck1-SH3.1 domain.The Journal of biological chemistry · 2020Article
- TCR Signaling: Mechanisms of Initiation and Propagation.Trends in biochemical sciences · 2018Review
- CD3ε Expression Defines Functionally Distinct Subsets of Vδ1 T Cells in Patients With Human Immunodeficiency Virus Infection.Frontiers in immunology · 2018Article
- Review
- Infectious pathogens may trigger specific allo-HLA reactivity via multiple mechanisms.Immunogenetics · 2017Review
- Lipid-dependent conformational dynamics underlie the functional versatility of T-cell receptor.Cell research · 2017Article
- Co-potentiation of antigen recognition: A mechanism to boost weak T cell responses and provide immunotherapy in vivo.Science advances · 2015Article
- TCR ITAM multiplicity is required for the generation of follicular helper T-cells.Nature communications · 2015Article
- Insights into the initiation of TCR signaling.Nature immunology · 2014Review
- Membrane association of the CD3ε signaling domain is required for optimal T cell development and function.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Article
- SLAP deficiency increases TCR avidity leading to altered repertoire and negative selection of cognate antigen-specific CD8+ T cells.Immunologic research · 2013Article
- Local autoantigen expression as essential gatekeeper of memory T-cell recruitment to islet grafts in diabetic hosts.Diabetes · 2013Article
- Nck recruitment to the TCR required for ZAP70 activation during thymic development.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
Abstract
Engagement of peptide-MHC by the TCR induces a conformational change in CD3epsilon that exposes a proline-rich sequence (PRS) and recruits the cytoskeletal adaptor Nck. This event, which precedes phosphorylation of the CD3epsilon ITAM, has been implicated in synapse formation and T cell function. However, there is compelling evidence that responsiveness to TCR ligation is CD3epsilon PRS independent. In this study, we show that the CD3epsilon PRS is necessary for peptide-MHC-induced phosphorylation of CD3epsilon and for recruitment of protein kinase Ctheta to the immune synapse in differentiated CD8+ T lymphocytes. However, whereas these two events are dispensable for functional T cell responsiveness to high-avidity ligands, they are required for responsiveness to low-avidity ones. Thus, in at least certain T cell clonotypes, the CD3epsilon PRS amplifies weak TCR signals by promoting synapse formation and CD3epsilon phosphorylation.
Indexed as
Identifiers
What OpenQuestion holds
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.