Evidence map›Paper›PMID 39276348›Full record

ArticleCell reports2024

Ligand-induced segregation from large cell-surface phosphatases is a critical step in γδ TCR triggering.

Fenglei Li, Sobhan Roy, Jacob Niculcea, Keith Gould, Erin J Adams, P Anton van der Merwe, Kaushik Choudhuri

Erratum issuedAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed.

  1. Review
  2. Article
  3. γδ T Cells and Inborn Errors of Immunity.European journal of immunology · 2025
    Review
  4. Article
  5. Review
  6. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors.

Fenglei LiDepartment of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, MI 48109, USA; Department of Biochemistry, University of Utah School of Medicine, Salt Lake City, UT 84112, USA.
Sobhan RoyDepartment of Biochemistry and Molecular Biology, University of Chicago, Chicago, IL 60637, USA.
Jacob NiculceaDepartment of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
Keith GouldDepartment of Infectious Diseases, Imperial College London, London W2 1NY, UK.
Erin J AdamsDepartment of Biochemistry and Molecular Biology, University of Chicago, Chicago, IL 60637, USA.
P Anton van der MerweSir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, UK. Electronic address: anton.vandermerwe@path.ox.ac.uk.
Kaushik ChoudhuriDepartment of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, MI 48109, USA; Department of Biochemistry, University of Utah School of Medicine, Salt Lake City, UT 84112, USA. Electronic address: kaushik.choudhuri@biochem.utah.edu.

Funding

XenograftP30CA046592 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Eric R. Fearon · 1988 to 2026
$178.2M
Molecular and functional investigation of the role of CD1 in gamma delta T cell surveillanceR01AI155984 · NIAID · UNIVERSITY OF CHICAGO · PI ADAMS, ERIN JUNE · 2020 to 2024
$2.7M
CELL BIOLOGY AND MOLECULAR MECHANISMS OF HUMAN GAMMA/DELTA T CELL ACTIVATIONR01AI134999 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHOUDHURI, KAUSHIK · 2019 to 2023
$1.9M
CELLULAR AND MOLECULAR BASIS OF GAMMA/DELTA T CELL ANTIGEN RECOGNITIONR00AI093884 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHOUDHURI, KAUSHIK · 2015 to 2016
$474k
CELLULAR AND MOLECULAR BASIS OF GAMMA/DELTA T CELL ANTIGEN RECOGNITIONK99AI093884 · NIAID · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI CHOUDHURI, KAUSHIK · 2012 to 2013
$147k
NCI NIH HHS P30 CA046592NIAID NIH HHS K99 AI093884NIAID NIH HHS R00 AI093884NIAID NIH HHS R01 AI134999NIAID NIH HHS R01 AI155984Wellcome Trust
6 · The paper itself

Abstract

Gamma/delta (γδ) T cells are unconventional lymphocytes that recognize diverse ligands via somatically recombined T cell antigen receptors (γδ TCRs). The molecular mechanism by which ligand recognition initiates γδ TCR signaling, a process known as TCR triggering, remains elusive. Unlike αβ TCRs, γδ TCRs are not mechanosensitive and do not require co-receptors or typical binding-induced conformational changes for triggering. Here, we show that γδ TCR triggering by nonclassical MHC class Ib antigens, a major class of ligands recognized by γδ T cells, requires steric segregation of the large cell-surface phosphatases CD45 and CD148 from engaged TCRs at synaptic close-contact zones. Increasing access of these inhibitory phosphatases to sites of TCR engagement, by elongating MHC class Ib ligands or truncating CD45/148 ectodomains, abrogates TCR triggering and T cell activation. Our results identify a critical step in γδ TCR triggering and provide insight into the core triggering mechanism of endogenous and synthetic tyrosine-phosphorylated immunoreceptors.

Indexed as

Receptors, Antigen, T-Cell, gamma-deltaAnimalsHumansLeukocyte Common AntigensLigandsLymphocyte ActivationMicePhosphorylationT-LymphocytesLeukocyte Common AntigensLigandsReceptors, Antigen, T-Cell, gamma-deltaCD1dCP: Immunologynonclassical MHC antigensT22T cell receptortriggeringγδ T cell

Identifiers

PMID39276348
PMCPMC11452322

What OpenQuestion holds

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Registered trials

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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.