Evidence map›Paper›PMID 26692174›Full record

ArticleNature immunology2016

A septin requirement differentiates autonomous and contact-facilitated T cell proliferation.

Adriana M Mujal, Julia K Gilden, Audrey Gérard, Makoto Kinoshita, Matthew F Krummel

Abstract read
In one paragraph

Article in Nature immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 21% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Frontiers in cell and developmental biology · 2021
    Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Editorial: Emerging Functions of Septins.Frontiers in cell and developmental biology · 2017
    Article
  15. Regulation of Store-Operated CaFrontiers in cell and developmental biology · 2016
    Article
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

5 authors at 2 institutions in 2 countries.

Adriana M MujalDepartment of Pathology, University of California, San Francisco, San Francisco, California, USA.
Julia K GildenDepartment of Pathology, University of California, San Francisco, San Francisco, California, USA.
Audrey GérardDepartment of Pathology, University of California, San Francisco, San Francisco, California, USA.
Makoto KinoshitaDivision of Biological Sciences, Nagoya University Graduate School of Science, Nagoya, Japan.
Matthew F KrummelDepartment of Pathology, University of California, San Francisco, San Francisco, California, USA.
University of California, San Francisco · USNagoya University · JP

Funding

Research BaseP30DK063720 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI VAISSE, CHRISTIAN · 2003 to 2019
$21.8M
MOLECULAR AND CELLULAR IMMUNOLOGYT32AI007334 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CYSTER, JASON G · 1988 to 2023
$11.0M
Spatiotemporal Control of T cell Synapse Stabilization and SignalingR01AI052116 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KRUMMEL, MATTHEW F · 2002 to 2022
$8.3M
Manipulating collectivity and Niches for Developing CD8 ImmunityR01AI114787 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KRUMMEL, MATTHEW F · 2015 to 2019
$2.2M
NIAID NIH HHS R01 AI052116NIAID NIH HHS R01 AI114787NIAID NIH HHS R01AI52116NIAID NIH HHS T32 AI007334NIDDK NIH HHS P30 DK063720
6 · The paper itself

Abstract

T cell proliferation is initiated by T cell antigen receptor (TCR) triggering, soluble growth factors or both. In characterizing T cells lacking the septin cytoskeleton, we found that successful cell division has discrete septin-dependent and septin-independent pathways. Septin-deficient T cells failed to complete cytokinesis when prompted by pharmacological activation or cytokines. In contrast, cell division was not dependent on septins when cell-cell contacts, such as those with antigen-presenting cells, provided a niche. This septin-independent pathway was mediated by phosphatidylinositol-3-OH kinase activation through a combination of integrins and costimulatory signals. We were able to differentiate between cytokine- and antigen-driven expansion in vivo and thus show that targeting septins has strong potential to moderate detrimental bystander or homeostatic cytokine-driven proliferation without influencing expansion driven by conventional antigen-presentation.

Indexed as

AnimalsAntigen-Presenting CellsCalcium SignalingCD8-Positive T-LymphocytesCell ProliferationCytokinesCytokinesisFlow CytometryImmunoblottingIntegrinsLymphocyte ActivationMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMicroscopy, ConfocalCytokinesIntegrinsPhosphatidylinositol 3-KinasesReceptors, Antigen, T-CellSept7 protein, mouseSeptinsSTAT5 Transcription Factor

Identifiers

PMID26692174
PMCPMC4755847
OpenAlexW2256589189

What OpenQuestion holds

Textmetadata
LicenceTDM
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.