ArticleProceedings of the National Academy of Sciences of the United States of America2010
T-cell antagonism by short half-life pMHC ligands can be mediated by an efficient trapping of T-cell polarization toward the APC.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
16 citing papers in PubMed, 22 citations in OpenAlex.
- Fluctuations in T cell receptor and pMHC interactions regulate T cell activation.Journal of the Royal Society, Interface · 2022Article
- Cross-TCR Antagonism Revealed by Optogenetically Tuning the Half-Life of the TCR Ligand Binding.International journal of molecular sciences · 2021Article
- Modulation of Adaptive Immunity and Viral Infections by Ion Channels.Frontiers in physiology · 2021Review
- Conformational States Control Lck Switching between Free and Confined Diffusion Modes in T Cells.Biophysical journal · 2020Article
- Modulation of Immune Responses to Influenza A Virus Vaccines by Natural Killer T Cells.Frontiers in immunology · 2020Review
- Contribution of Resident Memory CD8Pathogens (Basel, Switzerland) · 2019Review
- Human Respiratory Syncytial Virus: Infection and Pathology.Seminars in respiratory and critical care medicine · 2016Review
- Identifying Individual T Cell Receptors of Optimal Avidity for Tumor Antigens.Frontiers in immunology · 2015Review
- Autoimmunity and tumor immunology: two facets of a probabilistic immune system.BMC systems biology · 2014Article
- Phenotypic models of T cell activation.Nature reviews. Immunology · 2014Review
- Optimizing NKT cell ligands as vaccine adjuvants.Immunotherapy · 2014Review
- Human metapneumovirus keeps dendritic cells from priming antigen-specific naive T cells.Immunology · 2013Article
- Modulation of tumor immunity by soluble and membrane-bound molecules at the immunological synapse.Clinical & developmental immunology · 2013Review
- Interplay between T cell receptor binding kinetics and the level of cognate peptide presented by major histocompatibility complexes governs CD8+ T cell responsiveness.The Journal of biological chemistry · 2012Article
- Receptor signaling clusters in the immune synapse.Annual review of biophysics · 2012Review
- Opposite effects of endogenous peptide-MHC class I on T cell activity in the presence and absence of CD8.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
T-cell activation results from productive T-cell receptor (TCR) engagement by a cognate peptide-MHC (pMHC) complex on the antigen presenting cell (APC) surface, a process leading to the polarization of the T-cell secretory machinery toward the APC interface. We have previously shown that the half-life of the TCR/pMHC interaction and the density of pMHC on the APC are two parameters determining T-cell activation. However, whether the half-life of the TCR/pMHC interaction can modulate the efficiency of T-cell secretory machinery polarization toward an APC still remains unclear. Here, by using altered peptide ligands conferring different half-lives to the TCR/pMHC interaction, we have tested how this parameter can control T-cell polarization. We observed that only TCR/pMHC interactions with intermediate half-lives can promote the assembly of synapses that lead to T-cell activation. Strikingly, intermediate half-life interactions can be competed out by short half-life interactions, which can efficiently promote T-cell polarization and antagonize T-cell activation that was induced by activating intermediate half-life interactions. However, short TCR/pMHC interactions fail at promoting phosphorylation of signaling molecules at the T-cell-APC contact interface, which are needed for T-cell activation. Our data suggest that although intermediate half-life pMHC ligands promote assembly of activating synapses, this process can be inhibited by short half-life antagonistic pMHC ligands, which promote the assembly of non activating synapses.
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.