Evidence map›Paper›PMID 23255359›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2013

Induction of rapid T cell death and phagocytic activity by Fas-deficient lpr macrophages.

Ritsuko Oura, Rieko Arakaki, Akiko Yamada, Yasusei Kudo, Eiji Tanaka, Yoshio Hayashi, Naozumi Ishimaru

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.3field-weighted citation impact, top 41% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. Crosstalk between Fas and S1PThe Japanese dental science review · 2019
    Review
  3. Review
  4. 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

7 authors at 1 institution in 1 country.

Ritsuko OuraDepartment of Oral Molecular Pathology, Institute of Health Biosciences, University of Tokushima Graduate School, Tokushima 770-8504, Japan.
Rieko Arakaki
Akiko Yamada
Yasusei Kudo
Eiji Tanaka
Yoshio Hayashi
Naozumi Ishimaru
Tokushima University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Peripheral T cells are maintained by the apoptosis of activated T cells through the Fas-Fas ligand system. Although it is well known that normal T cells fail to survive in the Fas-deficient immune condition, the molecular mechanism for the phenomenon has yet to be elucidated. In this study, we demonstrate that rapid cell death and clearance of normal T cells were induced by Fas-deficient lpr macrophages. Transfer of normal T cells into lpr mice revealed that Fas expression on donor T cells was promptly enhanced through the IFN-γ/IFN-γR. In addition, Fas ligand expression and phagocytic activity of lpr macrophages were promoted through increased NF-κB activation. Controlling Fas expression on macrophages plays an essential role in maintaining T cell homeostasis in the peripheral immune system. Our data suggest a critical implication to the therapeutic strategies such as transplantation and immunotherapy for immune disorder or autoimmunity related to abnormal Fas expression.

Indexed as

AnimalsCell DeathCell MovementFas Ligand Proteinfas ReceptorGene Expression RegulationImmunomodulationMacrophagesMiceMice, Inbred MRL lprMice, TransgenicNF-kappa BPhagocytosisT-LymphocytesFas Ligand Proteinfas ReceptorNF-kappa B

Identifiers

PMID23255359
PMCPMC3539689
OpenAlexW2153209420

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.