Evidence map›Paper›PMID 35663975›Full record

ReviewFrontiers in immunology2022

The Role of M1/M2 Macrophage Polarization in Rheumatoid Arthritis Synovitis.

Maurizio Cutolo, Rosanna Campitiello, Emanuele Gotelli, Stefano Soldano

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 380 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
380citing papers in PubMed, 2 pooled it
82.9field-weighted citation impact, top 1% 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

380 citing papers in PubMed, 2 syntheses or guidelines pooled it, 549 citations in OpenAlex.

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320 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Maurizio CutoloLaboratory of Experimental Rheumatology and Academic Division of Clinical Rheumatology, Department of Internal Medicine and Specialties (DIMI), University of Genova, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) San Martino Polyclinic Hospital, Genoa, Italy.
Rosanna CampitielloLaboratory of Experimental Rheumatology and Academic Division of Clinical Rheumatology, Department of Internal Medicine and Specialties (DIMI), University of Genova, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) San Martino Polyclinic Hospital, Genoa, Italy.
Emanuele GotelliLaboratory of Experimental Rheumatology and Academic Division of Clinical Rheumatology, Department of Internal Medicine and Specialties (DIMI), University of Genova, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) San Martino Polyclinic Hospital, Genoa, Italy.
Stefano SoldanoLaboratory of Experimental Rheumatology and Academic Division of Clinical Rheumatology, Department of Internal Medicine and Specialties (DIMI), University of Genova, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) San Martino Polyclinic Hospital, Genoa, Italy.
Ospedale Policlinico San Martino · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Innate and adaptive immunity represent a harmonic counterbalanced system involved in the induction, progression, and possibly resolution of the inflammatory reaction that characterize autoimmune rheumatic diseases (ARDs), including rheumatoid arthritis (RA). Although the immunopathophysiological mechanisms of the ARDs are not fully clarified, they are often associated with an inappropriate macrophage/T-cell interaction, where classical (M1) or alternative (M2) macrophage activation may influence the occurrence of T-helper (Th)1 or Th2 responses. In RA patients, M1/Th1 activation occurs in an inflammatory environment dominated by Toll-like receptor (TLR) and interferon (IFN) signaling, and it promotes a massive production of pro-inflammatory cytokines [i.e., tumor necrosis factor-α (TNFα), interleukin (IL)-1, IL-12, IL-18, and IFNγ], chemotactic factors, and matrix metalloproteinases resulting in osteoclastogenesis, erosion, and progressive joint destruction. On the other hand, the activation of M2/Th2 response determines the release of growth factors and cytokines [i.e., IL-4, IL-10, IL-13, and transforming growth factor (TGF)-β] involved in the anti-inflammatory process leading to the clinical remission of RA. Several subtypes of macrophages have been described. Five polarization states from M1 to M2 have been confirmed in

Indexed as

Arthritis, RheumatoidAutoimmune DiseasesRespiratory Distress SyndromeSynovitisBiomarkersCytokinesHumansInflammationMacrophage ActivationMacrophagesBiomarkersCytokinesbDMARD therapyInflammationMacrophage polarizationRheumatoid anhritisSynovitis

Identifiers

PMID35663975
PMCPMC9161083
OpenAlexW4280542784

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.