Evidence map›Paper›PMID 26734459›Full record

ArticleImmunity, inflammation and disease2015

TNF and regulatory T cells are critical for sepsis-induced suppression of T cells.

David Stieglitz, Tobias Schmid, Nirav F Chhabra, Bernd Echtenacher, Daniela N Männel, Sven Mostböck

Open access · goldAbstract read
In one paragraph

Article in Immunity, inflammation and disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

12 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. TNFR1 Signaling Contributes to T Cell Anergy DuringFrontiers in cellular and infection microbiology · 2018
    Article
  9. Article
  10. Article
  11. Review
  12. 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 1 institution in 1 country.

David StieglitzInstitute of Immunology University of Regensburg Regensburg Germany.
Tobias SchmidInstitute of Immunology University of Regensburg Regensburg Germany.
Nirav F ChhabraInstitute of Immunology University of Regensburg Regensburg Germany.
Bernd EchtenacherInstitute of Immunology University of Regensburg Regensburg Germany.
Daniela N MännelInstitute of Immunology University of Regensburg Regensburg Germany.
Sven MostböckInstitute of Immunology University of Regensburg Regensburg Germany.
University of Regensburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The immune system in sepsis is impaired as seen by reduced numbers and function of immune cells and impaired antigen-specific antibody responses. We studied T cell function in septic mice using cecal ligation and puncture (CLP) as a clinically relevant mouse model for sepsis. The proliferative response of CD4(+) and CD8(+) T cells was suppressed in septic mice. Adoptive transfer experiments demonstrated that the T cells were not intrinsically altered by CLP. Instead, the septic host environment was responsible for this T cell suppression. While CLP-induced suppression was dependent on TNF activity, neither the activation of TNF receptors type 1 nor TNF receptor type 2 alone was sufficient to generate sepsis-induced suppression showing that the two TNF receptors can substitute each other. Specific depletion of regulatory T (Treg) cells improved the impaired T cell proliferation in septic recipients demonstrating participation of Treg in sepsis-induced suppression. In summary, sepsis leads to TNF-dependent suppression of T cell proliferation in vivo involving induction of Treg cells.

Indexed as

Immunosuppressionsuppressor cellsTNF receptorsTreg

Identifiers

PMID26734459
PMCPMC4693718
OpenAlexW1894084748

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.