Evidence map›Paper›PMID 27977740›Full record

ArticlePloS one2016

All Trans Retinoic Acid, Transforming Growth Factor β and Prostaglandin E2 in Mouse Plasma Synergize with Basophil-Secreted Interleukin-4 to M2 Polarize Murine Macrophages.

Victor W Ho, Elyse Hofs, Ingrid Elisia, Vivian Lam, Brian E Hsu, June Lai, Beryl Luk, Ismael Samudio, Gerald Krystal

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Immunometabolic effects ofImmunometabolism (Cobham, Surrey) · 2024
    Review
  3. Article
  4. Review
  5. Article
  6. Basophils as a potential therapeutic target in cancer.Journal of Zhejiang University. Science. B · 2021
    Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. 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 at 1 institution in 1 country.

Victor W HoThe Terry Fox Laboratory, British Columbia Cancer Agency, Vancouver, British Columbia, Canada.
Elyse HofsThe Terry Fox Laboratory, British Columbia Cancer Agency, Vancouver, British Columbia, Canada.
Ingrid ElisiaThe Terry Fox Laboratory, British Columbia Cancer Agency, Vancouver, British Columbia, Canada.
Vivian LamThe Terry Fox Laboratory, British Columbia Cancer Agency, Vancouver, British Columbia, Canada.
Brian E HsuThe Terry Fox Laboratory, British Columbia Cancer Agency, Vancouver, British Columbia, Canada.
June LaiThe Terry Fox Laboratory, British Columbia Cancer Agency, Vancouver, British Columbia, Canada.
Beryl LukThe Terry Fox Laboratory, British Columbia Cancer Agency, Vancouver, British Columbia, Canada.
Ismael SamudioThe Terry Fox Laboratory, British Columbia Cancer Agency, Vancouver, British Columbia, Canada.
Gerald KrystalThe Terry Fox Laboratory, British Columbia Cancer Agency, Vancouver, British Columbia, Canada.
BC Cancer Agency · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In previous studies we found that macrophages (MФs) from SH2-containing inositol-5'-phosphatase (SHIP) deficient mice are M2 polarized while their wild type (WT) counterparts are M1 polarized and that this difference in MФ phenotype can be recapitulated during in vitro derivation from bone marrow if mouse plasma (MP), but not fetal calf serum, is added to standard M-CSF-containing cultures. In the current study we investigated the mechanism by which MP skews SHIP-/- but not +/+ MФs to an M2 phenotype. Our results suggest that SHIP-/- basophils constitutively secrete higher levels of IL-4 than SHIP+/+ basophils and this higher level of IL-4 is sufficient to skew both SHIP+/+ and SHIP-/- MФs to an M2 phenotype, but only when MP is present to increase the sensitivity of the MФs to this level of IL-4. MP increases the IL-4 sensitivity of both SHIP+/+ and -/- MФs not by increasing cell surface IL-4 or CD36 receptor levels, but by triggering the activation of Erk and Akt and the production of ROS, all of which play a critical role in sensitizing MФs to IL-4-induced M2 skewing. Studies to identify the factor(s) in MP responsible for promoting IL-4-induced M2 skewing suggests that all-trans retinoic acid (ATRA), TGFβ and prostaglandin E2 (PGE2) all play a role. Taken together, these results indicate that basophil-secreted IL-4 plays an essential role in M2 skewing and that ATRA, TGFβ and PGE2 within MP collaborate to dramatically promote M2 skewing by acting directly on MФs to increase their sensitivity to IL-4.

Indexed as

AnimalsBasophilsCells, CulturedDinoprostoneInterleukin-4Macrophage ActivationMacrophagesMiceMice, Inbred C57BLMice, KnockoutPhosphatidylinositol-3,4,5-Trisphosphate 5-PhosphatasesPlasmaTransforming Growth Factor betaTretinoinDinoprostoneInterleukin-4Phosphatidylinositol-3,4,5-Trisphosphate 5-PhosphatasesTransforming Growth Factor betaTretinoin

Identifiers

PMID27977740
PMCPMC5158015
OpenAlexW2562718916

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.