Evidence map›Paper›PMID 29202478›Full record

ArticleThe Journal of clinical investigation2018

γδTCR recruits the Syk/PI3K axis to drive proinflammatory differentiation program.

Ryunosuke Muro, Takeshi Nitta, Kenta Nakano, Tadashi Okamura, Hiroshi Takayanagi, Harumi Suzuki

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.5field-weighted citation impact, top 19% of its field
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

32 citing papers in PubMed, 54 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. HEB collaborates with TCR signaling to upregulatebioRxiv : the preprint server for biology · 2025
    Article
  5. Review
  6. γδ T Cells and Inborn Errors of Immunity.European journal of immunology · 2025
    Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. New small molecules in dermatology: for the autoimmunity, inflammation and beyond.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Review
  14. Article
  15. Review
  16. Article
  17. RNA mProceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  18. Article
  19. Article
  20. Akt isoforms in the immune system.Frontiers in immunology · 2022
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 2 countries.

Ryunosuke MuroDepartment of Immunology and Pathology, Research Institute, National Center for Global Health and Medicine, Chiba, Japan.
Takeshi NittaDepartment of Immunology, Graduate School of Medicine and Faculty of Medicine, The University of Tokyo, Tokyo, Japan.
Kenta NakanoDepartment of Laboratory Animal Medicine, and.
Tadashi OkamuraDepartment of Laboratory Animal Medicine, and.
Hiroshi TakayanagiDepartment of Immunology, Graduate School of Medicine and Faculty of Medicine, The University of Tokyo, Tokyo, Japan.
Harumi SuzukiDepartment of Immunology and Pathology, Research Institute, National Center for Global Health and Medicine, Chiba, Japan.
National Center for Global Health and Medicine · JPThe University of Tokyo · JPInstitute of Laboratory Animal Science · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

γδT cells produce inflammatory cytokines and have been implicated in the pathogenesis of cancer, infectious diseases, and autoimmunity. The T cell receptor (TCR) signal transduction that specifically regulates the development of IL-17-producing γδT (γδT17) cells largely remains unclear. Here, we showed that the receptor proximal tyrosine kinase Syk is essential for γδTCR signal transduction and development of γδT17 in the mouse thymus. Zap70, another tyrosine kinase essential for the development of αβT cells, failed to functionally substitute for Syk in the development of γδT17. Syk induced the activation of the PI3K/Akt pathway upon γδTCR stimulation. Mice deficient in PI3K signaling exhibited a complete loss of γδT17, without impaired development of IFN-γ-producing γδT cells. Moreover, γδT17-dependent skin inflammation was ameliorated in mice deficient in RhoH, an adaptor known to recruit Syk. Thus, we deciphered lineage-specific TCR signaling and identified the Syk/PI3K pathway as a critical determinant of proinflammatory γδT cell differentiation.

Indexed as

AnimalsCell DifferentiationInflammationInterferon-gammaMiceMice, KnockoutPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, Antigen, T-Cell, gamma-deltaSignal TransductionSyk KinaseTh17 CellsIFNG protein, mouseInterferon-gammaPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, Antigen, T-Cell, gamma-deltaSyk KinaseSyk protein, mouseCell BiologyCytokinesImmunologySignal transductionT cell development

Identifiers

PMID29202478
PMCPMC5749532
OpenAlexW2772946027

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.