Evidence map›Paper›PMID 37583360›Full record

ArticleClinical and experimental immunology2024

IAPs and RIPK1 mediate LPS-induced cytokine production in healthy subjects and Crohn's disease.

Jakob Benedict Seidelin, Simone Jensen, Morten Hansen, Mariana Rodrigues de Carvalho Bronze, Delphine Cuchet-Lourenҫo, Sergey Nejentsev, Eric Charles LaCasse, Ole Haagen Nielsen

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Clinical and experimental immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.9field-weighted citation impact, top 20% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Review
  2. Article
  3. 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

8 authors at 3 institutions in 4 countries.

Jakob Benedict SeidelinDepartment of Gastroenterology, Medical Section, Herlev Hospital, University of Copenhagen, Denmark.ORCID 0000-0003-3230-7966
Simone JensenDepartment of Gastroenterology, Medical Section, Herlev Hospital, University of Copenhagen, Denmark.
Morten HansenDepartment of Oncology, Center for Cancer Immune Therapy, Herlev Hospital, University of Copenhagen, Denmark.
Mariana Rodrigues de Carvalho BronzeDepartment of Gastroenterology, Medical Section, Herlev Hospital, University of Copenhagen, Denmark.
Delphine Cuchet-LourenҫoDepartment of Medicine, University of Cambridge, Addenbrooke's Hospital, Cambridge, UK.
Sergey NejentsevDepartment of Medicine, University of Cambridge, Addenbrooke's Hospital, Cambridge, UK.
Eric Charles LaCasseApoptosis Research Centre, Children's Hospital of Eastern Ontario Research Institute, Canada.
Ole Haagen NielsenDepartment of Gastroenterology, Medical Section, Herlev Hospital, University of Copenhagen, Denmark.
University of Copenhagen · DKUniversity of Cambridge · GBChildren's Hospital of Eastern Ontario · CA

Funding

National Institute for Health ResearchOntario Institute for Cancer Research 832721
6 · The paper itself

Abstract

Innate immune activity fuels intestinal inflammation in Crohn's disease (CD), an inflammatory bowel disease. Identification and targeting of new molecular regulators of the innate activity are warranted to control the disease. Inhibitor of apoptosis proteins (IAPs) regulate both cell survival and inflammatory signaling. We investigated the effects of IAP inhibition by second mitochondria-derived activator of caspases (SMAC) mimetics (SMs) on innate responses and cell death to pathogen-associated molecular patterns in peripheral blood mononuclear cells (PBMCs) and monocytes. IAPs inhibited lipopolysaccharide (LPS)-induced expression of proinflammatory interleukin (IL)-1β, IL-6. Likewise, LPS (but not muramyl dipeptide or Escherichia coli) induced TNF-α was inhibited in CD and control PBMCs. The SM effect was partially reversed by inhibition of receptor-interacting serine/threonine-protein kinase 1 (RIPK1). The effect was mainly cell death independent. Thus, IAP inhibition by SMs leads to reduced production of proinflammatory cytokines and may be considered in the efforts to develop new therapeutic strategies to control CD.

Indexed as

Crohn DiseaseCarrier ProteinsCytokinesHealthy VolunteersHumansLeukocytes, MononuclearLipopolysaccharidesReceptor-Interacting Protein Serine-Threonine KinasesTumor Necrosis Factor-alphaCarrier ProteinsCytokinesLipopolysaccharidesReceptor-Interacting Protein Serine-Threonine KinasesRIPK1 protein, humanTumor Necrosis Factor-alphaCrohn’s diseasehuman monocyte activationinhibitor of apoptosis proteinslipopolysaccharidereceptor-interacting serine/threonine-protein kinase 1

Identifiers

PMID37583360
PMCPMC10876114
OpenAlexW4385850399

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.