ArticleNature2012
Biophysical mechanism of T-cell receptor triggering in a reconstituted system.
Article in Nature, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 209 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
209 citing papers in PubMed, 336 citations in OpenAlex.
- LAT condensation gates PLCγ1 activation via bimodal LAT phosphorylation.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- A Generalization of the Ternary Binding Model to Membrane-Confined Systems With Finite Copy Number.CPT: pharmacometrics & systems pharmacology · 2026Article
- Studying Macromolecular Composition in Cell-Cell Interfaces Using 3D Membrane Reconstitution Systems.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Spatial regulation of Lck activation at the CD8 immune synapse revealed by a FRET-Based biosensor.Cellular and molecular life sciences : CMLS · 2026Article
- Mechanotransduction through T cell receptors: consensus, controversies and future outlooks.Experimental & molecular medicine · 2026Review
- The resting and ligand-bound states of the membrane-embedded human T-cell receptor-CD3 complex.Nature communications · 2025Article
- PROTEIN-PROTEIN INTERACTION NETWORKS CAN BE HIGHLY SENSITIVE TO THE MEMBRANE PHASE TRANSITION.bioRxiv : the preprint server for biology · 2025Article
- Protein-protein interaction networks can be highly sensitive to the membrane phase transition.ArXiv · 2025Article
- Mechanoregulation of lymphocyte cytotoxicity.Nature reviews. Immunology · 2025Review
- Mimicking the TCR immune synapse for improved CAR-T cell function.Cell research · 2025Article
- Proofreading and single-molecule sensitivity in T cell receptor signaling by condensate nucleation.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Genetic Code Expansion: Recent Developments and Emerging Applications.Chemical reviews · 2025Review
- Comprehensive self-antigen screening to assess cross-reactivity in promiscuous T-cell receptors.Frontiers in immunology · 2025Article
- Development and validation of prognostic and diagnostic models utilizing immune checkpoint-related genes in public datasets for clear cell renal cell carcinoma.Frontiers in genetics · 2025Article
- Biochemical and biophysical mechanisms macrophages use to tune phagocytic appetite.Journal of cell science · 2025Review
- CAR-T cell therapy for the treatment of adult high-grade gliomas.NPJ precision oncology · 2024Review
- Prior Fc receptor activation primes macrophages for increased sensitivity to IgG via long-term and short-term mechanisms.Developmental cell · 2024Article
- Quantifying T cell receptor mechanics at membrane junctions using DNA origami tension sensors.Nature nanotechnology · 2024Article
- Differential roles of kinetic on- and off-rates in T-cell receptor signal integration revealed with a modified Fab'-DNA ligand.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Ligand requirements for immunoreceptor triggering.Communications biology · 2024Article
149 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
A T-cell-mediated immune response is initiated by the T-cell receptor (TCR) interacting with peptide-bound major histocompatibility complex (pMHC) on an infected cell. The mechanism by which this interaction triggers intracellular phosphorylation of the TCR, which lacks a kinase domain, remains poorly understood. Here, we have introduced the TCR and associated signalling molecules into a non-immune cell and reconstituted ligand-specific signalling when these cells are conjugated with antigen-presenting cells. We show that signalling requires the differential segregation of a phosphatase and kinase in the plasma membrane. An artificial, chemically controlled receptor system generates the same effect as TCR–pMHC, demonstrating that the binding energy of an extracellular protein–protein interaction can drive the spatial segregation of membrane proteins without a transmembrane conformational change. This general mechanism may extend to other receptors that rely on extrinsic kinases, including, as we demonstrate, chimaeric antigen receptors being developed for cancer immunotherapy.
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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.