Evidence map›Paper›PMID 39213151›Full record

ArticleCell reports2024

CD14 is a decision-maker between Fas-mediated death and inflammation.

Zoie Magri, David Jetton, Hayley I Muendlein, Wilson M Connolly, Hunter Russell, Irina Smirnova, Shruti Sharma, Stephen Bunnell, Alexander Poltorak

Abstract read
In one paragraph

Article in Cell reports, 2024. 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
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.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. 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

9 authors.

Zoie MagriGraduate Program in Immunology, Tufts Graduate School of Biomedical Sciences, Boston, MA 02111, USA.
David JettonGraduate Program in Immunology, Tufts Graduate School of Biomedical Sciences, Boston, MA 02111, USA.
Hayley I MuendleinDepartment of Immunology, Tufts University School of Medicine, Boston, MA 02111, USA.
Wilson M ConnollyDepartment of Immunology, Tufts University School of Medicine, Boston, MA 02111, USA.
Hunter RussellGraduate Program in Genetics, Molecular & Cellular Biology, Tufts Graduate School of Biomedical Sciences, Boston, MA 02111, USA.
Irina SmirnovaDepartment of Immunology, Tufts University School of Medicine, Boston, MA 02111, USA.
Shruti SharmaDepartment of Immunology, Tufts University School of Medicine, Boston, MA 02111, USA.
Stephen BunnellDepartment of Immunology, Tufts University School of Medicine, Boston, MA 02111, USA. Electronic address: stephen.bunnell@tufts.edu.
Alexander PoltorakDepartment of Immunology, Tufts University School of Medicine, Boston, MA 02111, USA. Electronic address: alexander.poltorak@tufts.edu.

Funding

Hyper-Responsiveness to TLR Agonists in Wild Derived MiceR01AI056234 · NIAID · TUFTS UNIVERSITY BOSTON · PI POLTORAK, ALEXANDER · 2003 to 2023
$8.4M
Regulation of LPS-responses by ZBP1R01AI167245 · NIAID · TUFTS UNIVERSITY BOSTON · PI POLTORAK, ALEXANDER · 2021 to 2025
$3.6M
Intracellular nucleic acid sensing and age-related chronic inflammationR01AI142005 · NIAID · TUFTS UNIVERSITY BOSTON · PI SHARMA, SHRUTI · 2019 to 2023
$2.3M
CD14 collaborates with TRIF to mediate septic responses downstream of TNF receptorsR21AI176055 · NIAID · TUFTS UNIVERSITY BOSTON · PI BUNNELL, STEPHEN C · 2024 to 2025
$446k
Hyper-Responsiveness to TLR Agonists in Wild Derived MiceR56AI056234 · NIAID · TUFTS UNIVERSITY BOSTON · PI POLTORAK, ALEXANDER · 2008 to 2008
$411k
Cytosolic DNA sensing instructs resident macrophage vitality and organismal longevityR56AG082812 · NIA · TUFTS UNIVERSITY BOSTON · PI SHARMA, SHRUTI · 2023 to 2023
$409k
NIAID NIH HHS R01 AI056234NIAID NIH HHS R01 AI142005NIAID NIH HHS R01 AI167245NIAID NIH HHS R21 AI176055NIAID NIH HHS R56 AI056234NIA NIH HHS R56 AG082812
6 · The paper itself

Abstract

Signaling through classical death receptor Fas was mainly appreciated as a pro-death pathway until recent reports characterized pro-inflammatory outcomes of Fas-mediated activation in pathological contexts. How Fas signaling can switch to pro-inflammatory activation is poorly understood. Herein, we report that in macrophages and neutrophils, the Toll-like receptor (TLR) adapter CD14 determines the inflammatory output of Fas-mediated signaling. Our findings propose CD14 as a crucial chaperone of Fas receptor internalization in macrophages and neutrophils, resulting in Cd14

Indexed as

fas ReceptorInflammationLipopolysaccharide ReceptorsMacrophagesSignal TransductionAdaptor Proteins, Vesicular TransportAnimalsApoptosisFas Ligand ProteinHumansMiceMice, Inbred C57BLNeutrophilsNF-kappa BAdaptor Proteins, Vesicular TransportFas Ligand ProteinFas protein, mousefas ReceptorLipopolysaccharide ReceptorsNF-kappa BTicam1 protein, mouseapoptosisCD14CP: ImmunologyFasinternalizationTRIF

Identifiers

PMID39213151
PMCPMC11471008

What OpenQuestion holds

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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.