Evidence map›Paper›PMID 25771769›Full record

ReviewClinical reviews in allergy & immunology2015

Etiologies of Sarcoidosis.

Edward S Chen, David R Moller

Abstract readReview
PubMed Publisher
In one paragraph

Review in Clinical reviews in allergy & immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed, 1 pooled it
9.4field-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

78 citing papers in PubMed, 1 synthesis or guideline pooled it, 157 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Residential fungal β-(1,3)-D-glucan exposure is associated with decreased pulmonary function in fibrotic pulmonary sarcoidosis.Sarcoidosis, vasculitis, and diffuse lung diseases : official journal of WASOG · 2025
    Article
  8. Particles exposures and sarcoidosis.Sarcoidosis, vasculitis, and diffuse lung diseases : official journal of WASOG · 2025
    Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Incidence, management and prognosis of new-onset sarcoidosis post COVID-19 infection.Sarcoidosis, vasculitis, and diffuse lung diseases : official journal of WASOG · 2024
    Article
  18. Article
  19. Article
  20. Article

18 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

2 authors at 1 institution in 1 country.

Edward S ChenDivision of Pulmonary and Critical Care Medicine, Department of Medicine, The Johns Hopkins University, 5501 Hopkins Bayview Circle, Baltimore, MD, 21224, USA, chenedwa@jhmi.edu.
David R Moller
Johns Hopkins University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Since sarcoidosis was first described more than a century ago, the etiologic determinants causing this disease remain uncertain. Studies suggest that genetic, host immunologic, and environmental factors interact together to cause sarcoidosis. Immunologic characteristics of sarcoidosis include non-caseating granulomas, enhanced local expression of T helper-1 (and often Th17) cytokines and chemokines, dysfunctional regulatory T-cell responses, dysregulated Toll-like receptor signaling, and oligoclonal expansion of CD4+ T cells consistent with chronic antigenic stimulation. Multiple environmental agents have been suggested to cause sarcoidosis. Studies from several groups implicate mycobacterial or propionibacterial organisms in the etiology of sarcoidosis based on tissue analyses and immunologic responses in sarcoidosis patients. Despite these studies, there is no consensus on the nature of a microbial pathogenesis of sarcoidosis. Some groups postulate sarcoidosis is caused by an active viable replicating infection while other groups contend there is no clinical, pathologic, or microbiologic evidence for such a pathogenic mechanism. The authors posit a novel hypothesis that proposes that sarcoidosis is triggered by a hyperimmune Th1 response to pathogenic microbial and tissue antigens associated with the aberrant aggregation of serum amyloid A within granulomas, which promotes progressive chronic granulomatous inflammation in the absence of ongoing infection.

Indexed as

CytokinesGene-Environment InteractionGene Expression RegulationGranulomaHLA AntigensHumansLymphocyte ActivationMycobacterium tuberculosisPropionibacterium acnesSarcoidosisSerum Amyloid A ProteinSignal TransductionTh17 CellsT-Lymphocytes, RegulatoryToll-Like ReceptorsCytokinesHLA AntigensSerum Amyloid A ProteinToll-Like Receptors

Identifiers

PMID25771769
OpenAlexW2052002232

What OpenQuestion 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 OpenQuestion graph.