Evidence map›Paper›PMID 40721670›Full record

ReviewNature reviews. Rheumatology2025

Dynamic macrophage phenotypes in autoimmune and inflammatory rheumatic diseases.

Maurizio Cutolo, Stefano Soldano, Vanessa Smith, Emanuele Gotelli, Elvis Hysa

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Rheumatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

41 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. CAR-macrophages: a new chapter in cancer immunotherapy.Acta biochimica et biophysica Sinica · 2026
    Article
  19. Review
  20. 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

5 authors.

Maurizio Cutolo *Laboratory of Experimental Rheumatology and Academic Division of Clinical Rheumatology, Department of Internal Medicine and Medical Specialties (DiMI), University of Genova, Genova, Italy. mcutolo@unige.it.ORCID http://orcid.org/0000-0002-5396-0932
Stefano Soldano *Laboratory of Experimental Rheumatology and Academic Division of Clinical Rheumatology, Department of Internal Medicine and Medical Specialties (DiMI), University of Genova, Genova, Italy.
Vanessa SmithDepartment of Rheumatology, Ghent University Hospital, University of Ghent, Ghent, Belgium.ORCID http://orcid.org/0000-0001-6271-7945
Emanuele GotelliLaboratory of Experimental Rheumatology and Academic Division of Clinical Rheumatology, Department of Internal Medicine and Medical Specialties (DiMI), University of Genova, Genova, Italy.ORCID http://orcid.org/0000-0002-4732-0306
Elvis HysaLaboratory of Experimental Rheumatology and Academic Division of Clinical Rheumatology, Department of Internal Medicine and Medical Specialties (DiMI), University of Genova, Genova, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrophages regulate inflammatory and fibrotic processes in several autoimmune and inflammatory rheumatic diseases. They are highly plastic cells, shifting within a range of pro-inflammatory and anti-inflammatory or pro-fibrotic phenotypes in response to dynamic interactions with other cells, environmental factors and cytokine signatures. The terms 'M1 macrophages', or classically activated, and 'M2 macrophages', or alternatively activated, were previously used to denote pro- and anti-inflammatory macrophage subsets, respectively, but this classification system has been outdated by in vivo evidence of a continuum of macrophage phenotypes that includes M1-like, M2-like and hybrid phenotypes. Deciphering the specific mechanisms that drive macrophage plasticity and function during the progression of rheumatoid arthritis, psoriatic arthritis, systemic sclerosis, systemic lupus erythematosus, and in synovitis and large vessel vasculitis in polymyalgia rheumatica and giant-cell arteritis, can improve our understanding of disease pathophysiology. Macrophage plasticity is enhanced in synovial tissue in rheumatoid arthritis, fibrotic skin and lung in systemic sclerosis, damaged kidney in systemic lupus erythematosus, and the bursal tissues or large vessels in polymyalgia rheumatica and giant-cell arteritis. Sophisticated transcriptomic analyses have revealed various phenotypic clusters of macrophages in biopsies of affected organs. Moreover, macrophage plasticity seems to be targeted by some standardized drugs used to treat the aforementioned conditions.

Indexed as

Autoimmune DiseasesInflammationMacrophagesRheumatic DiseasesHumansMacrophage ActivationPhenotype

Identifiers

What Socratic holds

Textmetadata
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.