Evidence map›Paper›PMID 33363531›Full record

ArticleFrontiers in immunology2020

Single Cell Transcriptomics Implicate Novel Monocyte and T Cell Immune Dysregulation in Sarcoidosis.

Lori Garman, Richard C Pelikan, Astrid Rasmussen, Caleb A Lareau, Kathryn A Savoy, Umesh S Deshmukh, Harini Bagavant, Albert M Levin, Salim Daouk, Wonder P Drake and 1 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 10% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. The inflammatory fingerprint reveals immune cell populations associated with disease activity in cardiac sarcoidosis.Clinical research in cardiology : official journal of the German Cardiac Society · 2026
    Article
  4. Cardiovascular Manifestations and Immunobiology of Sarcoidosis.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Review
  5. Article
  6. Article
  7. Immunopathogenesis of Sarcoidosis.Seminars in respiratory and critical care medicine · 2025
    Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Aberrant Lipid Metabolism in Macrophages Is Associated with Granuloma Formation in Sarcoidosis.American journal of respiratory and critical care medicine · 2024
    Article
  16. Phenotypes and Serum Biomarkers in Sarcoidosis.Diagnostics (Basel, Switzerland) · 2024
    Review
  17. Article
  18. Initial behaviors and attitudes towards the COVID-19 vaccine in sarcoidosis patients: results of a self-reporting questionnaire.Sarcoidosis, vasculitis, and diffuse lung diseases : official journal of WASOG · 2023
    Article
  19. Article
  20. Article
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

11 authors at 5 institutions in 1 country.

Lori GarmanOklahoma Medical Research Foundation, Genes and Human Disease, Oklahoma City, OK, United States.
Richard C PelikanOklahoma Medical Research Foundation, Genes and Human Disease, Oklahoma City, OK, United States.
Astrid RasmussenOklahoma Medical Research Foundation, Genes and Human Disease, Oklahoma City, OK, United States.
Caleb A LareauCell Circuits and Epigenomics Program, Broad Institute, Cambridge, MA, United States.
Kathryn A SavoyOklahoma Medical Research Foundation, Genes and Human Disease, Oklahoma City, OK, United States.
Umesh S DeshmukhOklahoma Medical Research Foundation, Arthritis and Clinical Immunology, Oklahoma City, OK, United States.
Harini BagavantOklahoma Medical Research Foundation, Arthritis and Clinical Immunology, Oklahoma City, OK, United States.
Albert M LevinDepartment of Public Health Sciences, Henry Ford Health System, Detroit, MI, United States.
Salim DaoukCardiovascular Institute, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States.
Wonder P DrakeVanderbilt University School of Medicine, Nashville, TN, United States.
Courtney G MontgomeryOklahoma Medical Research Foundation, Genes and Human Disease, Oklahoma City, OK, United States.
Oklahoma Medical Research Foundation · USBroad Institute · USHenry Ford Health System · USUniversity of Oklahoma Health Sciences Center · USVanderbilt University · US

Funding

Tracking and Evaluation CoreU54GM104938 · NIGMS · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI JUDITH A JAMES · 2013 to 2026
$68.2M
Comprehensive Genome Interrogation of African American Sarcoidosis FamiliesR01HL113326 · NHLBI · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI MONTGOMERY, COURTNEY · 2012 to 2022
$8.7M
Quantitative Analysis Core P30GM110766 · NIGMS · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI GAFFNEY, PATRICK M · 2014 to 2018
$6.1M
Microbial induction of sarcoidosis CD4+ T cell dysfunctionR01HL117074 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BERNARD, GORDON RAPHAEL, DRAKE, WONDER P. · 2013 to 2017
$3.8M
Mentoring in Translational Research in Interstitial Lung DiseasesK24HL127301 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Wonder P. Drake · 2016 to 2026
$1.2M
NHLBI NIH HHS K24 HL127301NHLBI NIH HHS R01 HL113326NHLBI NIH HHS R01 HL117074NIGMS NIH HHS P30 GM110766NIGMS NIH HHS U54 GM104938
6 · The paper itself

Abstract

Sarcoidosis is a systemic inflammatory disease characterized by infiltration of immune cells into granulomas. Previous gene expression studies using heterogeneous cell mixtures lack insight into cell-type-specific immune dysregulation. We performed the first single-cell RNA-sequencing study of sarcoidosis in peripheral immune cells in 48 patients and controls. Following unbiased clustering, differentially expressed genes were identified for 18 cell types and bioinformatically assessed for function and pathway enrichment. Our results reveal persistent activation of circulating classical monocytes with subsequent upregulation of trafficking molecules. Specifically, classical monocytes upregulated distinct markers of activation including adhesion molecules, pattern recognition receptors, and chemokine receptors, as well as enrichment of immunoregulatory pathways HMGB1, mTOR, and ephrin receptor signaling. Predictive modeling implicated TGFβ and mTOR signaling as drivers of persistent monocyte activation. Additionally, sarcoidosis T cell subsets displayed patterns of dysregulation. CD4 naïve T cells were enriched for markers of apoptosis and Th17/T

Indexed as

Gene Expression ProfilingSingle-Cell AnalysisTranscriptomeApoptosisBiomarkersCase-Control StudiesCell MovementClonal AnergyDisease ProgressionFemaleHumansImmunophenotypingMaleModels, BiologicalMonocytesOrgan SpecificityBiomarkersReceptors, Antigen, T-Cellcell migrationclassical monocyteslymphocyte activationregulatory T cellsRNA sequencing analysissarcoidosis

Identifiers

PMID33363531
PMCPMC7753017
OpenAlexW3111941790

What Socratic 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 Socratic graph.