Evidence map›Paper›PMID 38173720›Full record

ArticleFrontiers in immunology2023

FOXP3+ regulatory T cells are associated with the severity and prognosis of sarcoidosis.

Karen C Patterson, Wallace T Miller, Wayne W Hancock, Tatiana Akimova

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

10 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. New Therapies for Sarcoidosis: Molecular and Pathophysiological Basis.International journal of molecular sciences · 2026
    Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Immunopathogenesis of Sarcoidosis.Seminars in respiratory and critical care medicine · 2025
    Review
  10. 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

4 authors at 2 institutions in 1 country.

Karen C PattersonDivision of Pulmonary, Allergy, and Critical Care Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States.
Wallace T MillerDepartment of Radiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States.
Wayne W HancockDivision of Transplant Immunology, Department of Pathology and Laboratory Medicine, and Biesecker Center for Pediatric Liver Diseases, Children's Hospital of Philadelphia and Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States.
Tatiana AkimovaDivision of Transplant Immunology, Department of Pathology and Laboratory Medicine, and Biesecker Center for Pediatric Liver Diseases, Children's Hospital of Philadelphia and Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States.
University of Pennsylvania · USChildren's Hospital of Philadelphia · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rationale: Sarcoidosis is an inflammatory granulomatous disease of unknown etiology with predominant lung involvement. Organ involvement and disease severity, as well as the nature of immune alterations, vary among patients leading to a range of clinical phenotypes and outcomes. Our objective was to evaluate the association of disease course and immune responses in pulmonary sarcoidosis. Methods: In this prospective cohort study of 30 subjects, most of whom were followed for one year, we evaluated 14 inflammatory markers in plasma, 13 Treg/T cell flow cytometry markers and 8 parameters of FOXP3 Results: We identified a set of 13 immunological parameters that differ in sarcoidosis subjects in comparison with healthy donors. Five of those were inversely correlated with suppressive function of Tregs in sarcoidosis, and six (TNFα, TNFR I and II, sCD25, Ki-67 and number of Tregs) were particularly upregulated or increased in subjects with thoracic lymphadenopathy. Treg suppressive function was significantly lower in patients with thoracic lymphadenopathy, and in patients with higher burdens of pulmonary and systemic symptoms. A combination of five inflammatory markers, Ki-67 expression, Treg function, and lung diffusion capacity evaluated at study entry predicted need for therapy at one year follow-up in 90% of cases. Conclusion: Tregs may suppress ongoing inflammation at local and systemic levels, and TNFα, TNFR I and II, sCD25 and Ki-67 emerge as attractive biomarkers for

Indexed as

LymphadenopathySarcoidosisForkhead Transcription FactorsHumansKi-67 AntigenPrognosisProspective StudiesReceptors, Tumor Necrosis Factor, Type IT-Lymphocytes, RegulatoryTumor Necrosis Factor-alphaForkhead Transcription FactorsFOXP3 protein, humanKi-67 AntigenReceptors, Tumor Necrosis Factor, Type ITumor Necrosis Factor-alphaKi-67regulatory T-cellssarcoidosissCD25TNFRITNFRIITNFαTreg

Identifiers

PMID38173720
PMCPMC10761433
OpenAlexW4390007031

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.