Evidence map›Paper›PMID 26711346›Full record

ArticleCell reports2015

Disrupted PI3K p110δ Signaling Dysregulates Maternal Immune Cells and Increases Fetal Mortality In Mice.

Jens Kieckbusch, Elisa Balmas, Delia A Hawkes, Francesco Colucci

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

11 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Roles of Interferons in Pregnant Women with Dengue Infection: Protective or Dangerous Factors.The Canadian journal of infectious diseases & medical microbiology = Journal canadien des maladies infectieuses et de la microbiologie medicale · 2017
    Review
  11. 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

4 authors at 3 institutions in 1 country.

Jens KieckbuschDepartment of Obstetrics and Gynaecology, University of Cambridge School of Clinical Medicine, NIHR Cambridge Biomedical Research Centre, Addenbrooke's Hospital, Box 111, Hills Road, Cambridge CB2 0SP, UK; Centre for Trophoblast Research, University of Cambridge, Physiology Building, Downing Street, Cambridge CB2 3EG, UK.
Elisa BalmasDepartment of Obstetrics and Gynaecology, University of Cambridge School of Clinical Medicine, NIHR Cambridge Biomedical Research Centre, Addenbrooke's Hospital, Box 111, Hills Road, Cambridge CB2 0SP, UK; Centre for Trophoblast Research, University of Cambridge, Physiology Building, Downing Street, Cambridge CB2 3EG, UK.
Delia A HawkesDepartment of Obstetrics and Gynaecology, University of Cambridge School of Clinical Medicine, NIHR Cambridge Biomedical Research Centre, Addenbrooke's Hospital, Box 111, Hills Road, Cambridge CB2 0SP, UK.
Francesco ColucciDepartment of Obstetrics and Gynaecology, University of Cambridge School of Clinical Medicine, NIHR Cambridge Biomedical Research Centre, Addenbrooke's Hospital, Box 111, Hills Road, Cambridge CB2 0SP, UK; Centre for Trophoblast Research, University of Cambridge, Physiology Building, Downing Street, Cambridge CB2 3EG, UK. Electronic address: fc287@medschl.cam.ac.uk.
Addenbrooke's Hospital · GBNIHR Cambridge Biomedical Research CentreUniversity of Cambridge · GB

Funding

Wellcome TrustWellcome Trust 094073/Z/10/Z
6 · The paper itself

Abstract

Maternal immune cells are an integral part of reproduction, but how they might cause pregnancy complications remains elusive. Macrophages and their dual function in inflammation and tissue repair are thought to play key yet undefined roles. Altered perinatal growth underpins adult morbidity, and natural killer (NK) cells may sustain fetal growth by establishing the placental blood supply. Using a mouse model of genetic inactivation of PI3K p110δ, a key intracellular signaling molecule in leukocytes, we show that p110δ regulates macrophage dynamics and NK-cell-mediated arterial remodeling. The uterus of dams with inactive p110δ had decreased IFN-γ and MHC class II(low) macrophages but enhanced IL-6. Poor vascular remodeling and a pro-inflammatory uterine milieu resulted in fetal death or growth retardation. Our results provide one mechanism that explains how imbalanced adaptations of maternal innate immune cells to gestation affect offspring well-being with consequence perinatally and possibly into adulthood.

Indexed as

Fetal DeathAnimalsClass I Phosphatidylinositol 3-KinasesCytokinesDisease Models, AnimalFemaleFetal Growth RetardationGene SilencingInterferon-gammaKiller Cells, NaturalMacrophagesMicePhosphatidylinositol 3-KinasesPregnancySignal TransductionUterusClass I Phosphatidylinositol 3-KinasesCytokinesInterferon-gammaPhosphatidylinositol 3-KinasesPik3cd protein, mouse

Identifiers

PMID26711346
PMCPMC4700049
OpenAlexW2196569667

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.