Evidence map›Paper›PMID 24553452›Full record

ArticleScientific reports2014

Unique macrophages different from M1/M2 macrophages inhibit T cell mitogenesis while upregulating Th17 polarization.

Yutaka Tatano, Toshiaki Shimizu, Haruaki Tomioka

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

32 citing papers in PubMed, 58 citations in OpenAlex.

  1. Understanding Autoimmune Response Mechanisms in Leprosy.Indian dermatology online journal · 2025
    Article
  2. Review
  3. Holothurian triterpene glycoside cucumarioside ACancer cell international · 2023
    Article
  4. Article
  5. Macrophage Dysfunction in Autoimmune Rheumatic Diseases and Atherosclerosis.International journal of molecular sciences · 2022
    Review
  6. Review
  7. Article
  8. Macrophages as a "weapon" in anticancer cellular immunotherapy.The Kaohsiung journal of medical sciences · 2021
    Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Reactive oxygen species modulate macrophage immunosuppressive phenotype through the up-regulation of PD-L1.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  17. Article
  18. Review
  19. Article
  20. 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

3 authors at 1 institution in 1 country.

Yutaka TatanoDepartment of Microbiology and Immunology, Shimane University School of Medicine, Izumo, Shimane 693-8501, Japan.
Toshiaki ShimizuDepartment of Microbiology and Immunology, Shimane University School of Medicine, Izumo, Shimane 693-8501, Japan.
Haruaki TomiokaDepartment of Microbiology and Immunology, Shimane University School of Medicine, Izumo, Shimane 693-8501, Japan.
Shimane University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mycobacterial infection induces suppressor macrophages (MΦs), causing disease exacerbation. There are two major MΦ subsets (M1 and M2 MΦs) that are phenotypically and functionally different. Here, we examined which of the MΦ subsets the mycobacterial infection-induced suppressor MΦs (MIS-MΦs) belong to. MIS-MΦs down-regulated T cell production of Th1 and Th2 cytokines but markedly increased production of interleukin (IL)-17A and IL-22 through up-regulation of Th17 cell expansion. In this phenomenon, a novel MΦ population, which is functionally distinguishable from M1 and M2 MΦ subsets and possesses unique phenotypes (IL-12(+), IL-1β(high), IL-6(+), tumor necrosis factor (TNF)-α(+), nitric oxide synthase (NOS) 2(+), CCR7(high), IL-10(high), arginase (Arg)-1(-), mannose receptor (MR)(low), Ym1(high), Fizz(low), and CD163(high)), played central roles through the action of IL-6 and transforming growth factor (TGF)-β but not IL-21 and IL-23. This new type of MΦ population was induced in infected mice and actively supported the in vivo expansion of Th17 cells.

Indexed as

AnimalsCell PolarityCells, CulturedCoculture TechniquesCytokinesInterleukin-17Interleukin-22InterleukinsMacrophagesMaleMiceMice, Inbred BALB CMycobacterium InfectionsPhenotypeRNA, MessengerSpleenCytokinesInterleukin-17Interleukin-22InterleukinsRNA, Messenger

Identifiers

PMID24553452
PMCPMC3930092
OpenAlexW2066525789

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.