Evidence map›Paper›PMID 21356378›Full record

ArticleThe American journal of pathology2011

M2 polarized macrophages and giant cells contribute to myofibrosis in neuromuscular sarcoidosis.

Stefan Prokop, Frank L Heppner, Hans H Goebel, Werner Stenzel

Abstract read
In one paragraph

Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
–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

63 citing papers in PubMed.

  1. Specific Biomarkers Involved in Sarcoidosis Diagnosis and Prognosis.International journal of molecular sciences · 2026
    Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Bioinformatics analysis identifies candidate biomarkers associated with sarcoidosis.Sarcoidosis, vasculitis, and diffuse lung diseases : official journal of WASOG · 2025
    Article
  7. Immunopathogenesis of Sarcoidosis.Seminars in respiratory and critical care medicine · 2025
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Thoughts on the Etiology of Cherubism.Journal of clinical medicine · 2024
    Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Review

3 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.

Stefan ProkopDepartment of Neuropathology, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Frank L Heppner
Hans H Goebel
Werner Stenzel

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The etiopathogenesis of sarcoidosis, a systemic granulomatous disease, still remains obscure. A multitude of organs have been described to be affected in systemic sarcoidosis. Skeletal muscles may also be affected, leading to myalgia and weakness. A workup of the specific immune response with emphasis on the macrophage response is provided herein. Affected muscle tissue from seven patients with systemic sarcoidosis was analyzed and compared with that from seven patients with other myopathies containing macrophagocytic infiltration. Monocytes/macrophages and giant cells in granulomas of muscle tissue from patients with sarcoidosis show a status of alternative activation (M2) based on their expression of CD206, CD301, arginase-1, and suppressor of cytokine signaling-1 as a consequence of a functionally type 2 helper T cell (Th2)-biased cytokine profile. Significant fibrosis and up-regulation of CCL18 were associated with the M2 phenotype of macrophages. Conversely, up-regulated Th1 cytokines did not result in significant classical activation of macrophages (M1), with poor inducible nitric oxide synthase and cyclooxygenase-2 production. Giant cell formation was further associated with up-regulated expression of DNAX-activating protein of 12 kDa (DAP12; gene symbol TYROBP). Functionally, alternative activation of macrophages on the basis of a Th2-biased immune response may induce clinical symptoms and chronic evolution of neuromuscular sarcoidosis. This is the first characterization of Th2-mediated immune mechanisms in neuromuscular sarcoidosis suggesting that a specific macrophage activation status leading to myofibrosis may be a key event in the pathogenesis of this disease.

Indexed as

Cell PolarityMacrophage ActivationAgedChemokines, CCCytokinesEpithelial CellsFemaleFibrosisGene Expression RegulationGiant CellsGranulomaHumansMacrophagesMaleMiddle AgedMonocytesCCL18 protein, humanChemokines, CCCytokinesRNA, Messenger

Identifiers

PMID21356378
PMCPMC3069905

What OpenQuestion holds

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Registered trials

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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.