ArticleThe Journal of experimental medicine1998
Dissociation of intracellular signaling pathways in response to partial agonist ligands of the T cell receptor.
Article in The Journal of experimental medicine, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 86 citations in OpenAlex.
- Regulation of T Helper Cell Fate by TCR Signal Strength.Frontiers in immunology · 2020Review
- Review
- An Altered gp100 Peptide Ligand with Decreased Binding by TCR and CD8α Dissects T Cell Cytotoxicity from Production of Cytokines and Activation of NFAT.Frontiers in immunology · 2013Article
- Lck, Membrane Microdomains, and TCR Triggering Machinery: Defining the New Rules of Engagement.Frontiers in immunology · 2012Article
- Cells diversify transmembrane signaling through the controlled chaos of protein disorder.Self/nonself · 2011Article
- Differential occurrence of protein intrinsic disorder in the cytoplasmic signaling domains of cell receptors.Self/nonself · 2011Article
- The SCHOOL of nature: I. Transmembrane signaling.Self/nonself · 2010Article
- Structure-Function analysis of the CTLA-4 interaction with PP2A.BMC immunology · 2009Article
- The proline-rich sequence of CD3epsilon as an amplifier of low-avidity TCR signaling.Journal of immunology (Baltimore, Md. : 1950) · 2008Article
- SCHOOL model and new targeting strategies.Advances in experimental medicine and biology · 2008Review
- A conformational change senses the strength of T cell receptor-ligand interaction during thymic selection.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Regulation of T-cell activation by phosphodiesterase 4B2 requires its dynamic redistribution during immunological synapse formation.Molecular and cellular biology · 2003Article
- Allelic variation of MHC structure alters peptide ligands to induce atypical partial agonistic CD8+ T cell function.The Journal of experimental medicine · 2003Article
- Activation of human T cells by FcR nonbinding anti-CD3 mAb, hOKT3gamma1(Ala-Ala).The Journal of clinical investigation · 2003Article
- Surface cytotoxic T lymphocyte-associated antigen 4 partitions within lipid rafts and relocates to the immunological synapse under conditions of inhibition of T cell activation.The Journal of experimental medicine · 2002Article
- Zap-70-independent Ca(2+) mobilization and Erk activation in Jurkat T cells in response to T-cell antigen receptor ligation.Molecular and cellular biology · 2001Article
- Clonal anergy induced in a CD8+ hapten-specific cytotoxic T-cell clone by an altered hapten-peptide ligand.Immunology · 2001Article
- Crossreactive recognition of viral, self, and bacterial peptide ligands by human class I-restricted cytotoxic T lymphocyte clonotypes: implications for molecular mimicry in autoimmune disease.Proceedings of the National Academy of Sciences of the United States of America · 1999Article
- Preselection thymocytes are more sensitive to T cell receptor stimulation than mature T cells.The Journal of experimental medicine · 1998Article
- Respiratory syntycial virus: Current treatment strategies and vaccine approaches.Antiviral chemistry & chemotherapyReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The T cell receptor (TCR) is a versatile receptor able to generate different signals that result in distinct T cell responses. The pattern of early signals is determined by the TCR binding kinetics that control the ability of the ligand to coengage TCR and coreceptor. Coengagement of TCR and CD4 results in an agonist signaling pattern with complete tyrosine phosphorylation of TCR subunits, and recruitment and activation of ZAP-70. In contrast, TCR engagement without CD4 coengagement causes a partial agonist type of signaling, characterized by distinct phosphorylation of TCR subunits and recruitment but no activation of ZAP-70. The pathways triggered by partial agonist signaling are unknown. Here, we show that agonists cause association of active lck and active ZAP-70 with p120-GTPase-activating protein (p120-GAP). These associations follow engagement of CD4 or CD3, respectively. In contrast, partial agonists do not activate lck or ZAP-70, but induce association of p120-GAP with inactive ZAP-70. Despite these differences, both agonist and partial agonist signals activate the mitogen-activated protein kinase (MAPK) pathway. However, MAPK activation by partial agonists is transient, supporting a kinetic, CD4-dependent model for the mechanism of action of variant TCR ligands. Transient MAPK activation may explain some of the responses to TCR partial agonists and antagonists.
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.