Evidence map›Paper›PMID 36090971›Full record

ReviewFrontiers in immunology2022

Activation mechanisms of monocytes/macrophages in adult-onset Still disease.

Hiroto Tsuboi, Seiji Segawa, Mizuki Yagishita, Hirofumi Toko, Fumika Honda, Ayako Kitada, Haruka Miki, Ayako Ohyama, Shinya Hagiwara, Yuya Kondo and 2 more

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
7.1field-weighted citation impact, top 2% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Role ofCentral-European journal of immunology · 2025
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  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

12 authors at 1 institution in 1 country.

Hiroto TsuboiDepartment of Rheumatology, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan.
Seiji SegawaDepartment of Rheumatology, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan.
Mizuki YagishitaDepartment of Rheumatology, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan.
Hirofumi TokoDepartment of Rheumatology, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan.
Fumika HondaDepartment of Rheumatology, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan.
Ayako KitadaDepartment of Rheumatology, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan.
Haruka MikiDepartment of Rheumatology, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan.
Ayako OhyamaDepartment of Rheumatology, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan.
Shinya HagiwaraDepartment of Rheumatology, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan.
Yuya KondoDepartment of Rheumatology, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan.
Isao MatsumotoDepartment of Rheumatology, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan.
Takayuki SumidaDepartment of Rheumatology, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan.
University of Tsukuba · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adult onset Still disease (AOSD) is a systemic inflammatory disorder characterized by skin rash, spiking fever, arthritis, sore throat, lymphadenopathy, and hepatosplenomegaly. Although the etiology of this disease has not been fully clarified, both innate and acquired immune responses could contribute to its pathogenesis. Hyperactivation of macrophages and neutrophils along with low activation of natural killer (NK) cells in innate immunity, as well as hyperactivation of Th1 and Th17 cells, whereas low activation of regulatory T cells (Tregs) in acquired immunity are involved in the pathogenic process of AOSD. In innate immunity, activation of monocytes/macrophages might play central roles in the development of AOSD and macrophage activation syndrome (MAS), a severe life-threating complication of AOSD. Regarding the activation mechanisms of monocytes/macrophages in AOSD, in addition to type II interferon (IFN) stimulation, several pathways have recently been identified, such as the pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs)-pattern recognition receptors (PRRs) axis, and neutrophil extracellular traps (NETs)-DNA. These stimulations on monocytes/macrophages cause activation of the nucleotide-binding oligomerization domain, leucine-rich repeat, and pyrin domain (NLRP) 3 inflammasomes, which trigger capase-1 activation, resulting in conversion of pro-IL-1β and pro-IL-18 into mature forms. Thereafter, IL-1β and IL-18 produced by activated monocytes/macrophages contribute to various clinical features in AOSD. We identified placenta-specific 8 (PLAC8) as a specifically increased molecule in monocytes of active AOSD, which correlated with serum levels of CRP, ferritin, IL-1β, and IL-18. Interestingly, PLAC8 could suppress the synthesis of pro-IL-1β and pro-IL-18

Indexed as

Macrophage Activation SyndromeStill's Disease, Adult-OnsetHumansInterleukin-18MacrophagesMonocytesProteinsInterleukin-18PLAC8 protein, humanProteinsadult-onset still diseaseIL-18IL-1βinflammasomemonocytes/macrophagesplacenta-specific 8

Identifiers

PMID36090971
PMCPMC9461677
OpenAlexW4293116352

What Socratic 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 Socratic graph.