Evidence map›Paper›PMID 26734005›Full record

ReviewFrontiers in immunology2015

Naïve T Cell Homeostasis Regulated by Stress Responses and TCR Signaling.

Daisuke Kamimura, Toru Atsumi, Andrea Stofkova, Naoki Nishikawa, Takuto Ohki, Hironao Suzuki, Kokichi Katsunuma, Jing-Jing Jiang, Hidenori Bando, Jie Meng and 5 more

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. 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, top 92% 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

6 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. CRISPR/Cas9: A Powerful Strategy to Improve CAR-T Cell Persistence.International journal of molecular sciences · 2023
    Review
  6. 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

15 authors at 3 institutions in 1 country.

Daisuke KamimuraDivision of Molecular Neuroimmunology, Institute for Genomic Medicine, Graduate School of Medicine, Hokkaido University, Sapporo, Japan; Laboratory of Developmental Immunology, WPI Immunology Frontier Research Center, Graduate School of Frontier Biosciences, Osaka University, Suita, Japan; Laboratory of Developmental Immunology, WPI Immunology Frontier Research Center, Graduate School of Medicine, Osaka University, Suita, Japan.
Toru AtsumiDivision of Molecular Neuroimmunology, Institute for Genomic Medicine, Graduate School of Medicine, Hokkaido University, Sapporo, Japan; Laboratory of Developmental Immunology, WPI Immunology Frontier Research Center, Graduate School of Frontier Biosciences, Osaka University, Suita, Japan; Laboratory of Developmental Immunology, WPI Immunology Frontier Research Center, Graduate School of Medicine, Osaka University, Suita, Japan.
Andrea StofkovaDivision of Molecular Neuroimmunology, Institute for Genomic Medicine, Graduate School of Medicine, Hokkaido University , Sapporo , Japan.
Naoki NishikawaDivision of Molecular Neuroimmunology, Institute for Genomic Medicine, Graduate School of Medicine, Hokkaido University , Sapporo , Japan.
Takuto OhkiDivision of Molecular Neuroimmunology, Institute for Genomic Medicine, Graduate School of Medicine, Hokkaido University, Sapporo, Japan; Laboratory of Developmental Immunology, WPI Immunology Frontier Research Center, Graduate School of Frontier Biosciences, Osaka University, Suita, Japan; Laboratory of Developmental Immunology, WPI Immunology Frontier Research Center, Graduate School of Medicine, Osaka University, Suita, Japan.
Hironao SuzukiDivision of Molecular Neuroimmunology, Institute for Genomic Medicine, Graduate School of Medicine, Hokkaido University, Sapporo, Japan; Laboratory of Developmental Immunology, WPI Immunology Frontier Research Center, Graduate School of Frontier Biosciences, Osaka University, Suita, Japan; Laboratory of Developmental Immunology, WPI Immunology Frontier Research Center, Graduate School of Medicine, Osaka University, Suita, Japan.
Kokichi KatsunumaLaboratory of Developmental Immunology, WPI Immunology Frontier Research Center, Graduate School of Frontier Biosciences, Osaka University, Suita, Japan; Laboratory of Developmental Immunology, WPI Immunology Frontier Research Center, Graduate School of Medicine, Osaka University, Suita, Japan.
Jing-Jing JiangDivision of Molecular Neuroimmunology, Institute for Genomic Medicine, Graduate School of Medicine, Hokkaido University, Sapporo, Japan; Laboratory of Developmental Immunology, WPI Immunology Frontier Research Center, Graduate School of Frontier Biosciences, Osaka University, Suita, Japan; Laboratory of Developmental Immunology, WPI Immunology Frontier Research Center, Graduate School of Medicine, Osaka University, Suita, Japan.
Hidenori BandoDivision of Molecular Neuroimmunology, Institute for Genomic Medicine, Graduate School of Medicine, Hokkaido University, Sapporo, Japan; Laboratory of Developmental Immunology, WPI Immunology Frontier Research Center, Graduate School of Frontier Biosciences, Osaka University, Suita, Japan; Laboratory of Developmental Immunology, WPI Immunology Frontier Research Center, Graduate School of Medicine, Osaka University, Suita, Japan.
Jie MengDivision of Molecular Neuroimmunology, Institute for Genomic Medicine, Graduate School of Medicine, Hokkaido University, Sapporo, Japan; Laboratory of Developmental Immunology, WPI Immunology Frontier Research Center, Graduate School of Frontier Biosciences, Osaka University, Suita, Japan; Laboratory of Developmental Immunology, WPI Immunology Frontier Research Center, Graduate School of Medicine, Osaka University, Suita, Japan.
Lavannya SabharwalDivision of Molecular Neuroimmunology, Institute for Genomic Medicine, Graduate School of Medicine, Hokkaido University, Sapporo, Japan; Laboratory of Developmental Immunology, WPI Immunology Frontier Research Center, Graduate School of Frontier Biosciences, Osaka University, Suita, Japan; Laboratory of Developmental Immunology, WPI Immunology Frontier Research Center, Graduate School of Medicine, Osaka University, Suita, Japan.
Hideki OguraDivision of Molecular Neuroimmunology, Institute for Genomic Medicine, Graduate School of Medicine, Hokkaido University, Sapporo, Japan; Laboratory of Developmental Immunology, WPI Immunology Frontier Research Center, Graduate School of Frontier Biosciences, Osaka University, Suita, Japan; Laboratory of Developmental Immunology, WPI Immunology Frontier Research Center, Graduate School of Medicine, Osaka University, Suita, Japan.
Toshio HiranoOsaka University , Suita , Japan.
Yasunobu ArimaDivision of Molecular Neuroimmunology, Institute for Genomic Medicine, Graduate School of Medicine, Hokkaido University, Sapporo, Japan; Laboratory of Developmental Immunology, WPI Immunology Frontier Research Center, Graduate School of Frontier Biosciences, Osaka University, Suita, Japan; Laboratory of Developmental Immunology, WPI Immunology Frontier Research Center, Graduate School of Medicine, Osaka University, Suita, Japan.
Masaaki MurakamiDivision of Molecular Neuroimmunology, Institute for Genomic Medicine, Graduate School of Medicine, Hokkaido University, Sapporo, Japan; Laboratory of Developmental Immunology, WPI Immunology Frontier Research Center, Graduate School of Frontier Biosciences, Osaka University, Suita, Japan; Laboratory of Developmental Immunology, WPI Immunology Frontier Research Center, Graduate School of Medicine, Osaka University, Suita, Japan.
Osaka University · JPHokkaido University · JPUbe Frontier University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The survival of naïve T cells is believed to require signals from TCR-pMHC interactions and cytokines such as IL-7. In contrast, signals that negatively impact naïve T cell survival are less understood. We conducted a forward genetic screening of mice and found a mutant mouse line with reduced number of naïve T cells (T-Red mice). T-Red mice have a point mutation in the Kdelr1 gene, and their naïve T cells show enhanced integrated stress response (ISR), which eventually induces their apoptosis. Therefore, naïve T cells require a KDEL receptor-mediated mechanism that efficiently relieves cellular stress for their survival in vivo. Interestingly, naïve T cells expressing TCR with higher affinity/avidity to self-antigens survive in T-Red mice, suggesting the possible link between TCR-mediated survival and ISR-induced apoptosis. In this article, we discuss the regulation of naïve T cell homeostasis, keeping special attention on the ISR and TCR signal.

Indexed as

mutagenesisnaive T cellsstress responseT cell homeostasisTCR signaling

Identifiers

PMID26734005
PMCPMC4681834
OpenAlexW2206985943

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.