Evidence map›Paper›PMID 26223504›Full record

ReviewSeminars in immunopathology2015

Gene expression profiling offers insights into the role of innate immune signaling in SSc.

Michael E Johnson, Patricia A Pioli, Michael L Whitfield

Registry-linked trialOpen access · greenAbstract readReview
In one paragraph

Review in Seminars in immunopathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04630782 (Precision Medicine in Systemic Sclerosis Gastrointestinal Disease), which is not on this map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.5field-weighted citation impact, top 8% 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.

NCT04630782 unknown statusnot on this mapstarted 2020, after this paper: background citation

Precision Medicine in Systemic Sclerosis Gastrointestinal Disease: Evaluating Imaging and Stool Biomarkers for Differentiating Disease Stages and Treatment Responses

TypeobservationalSponsorSingapore General HospitalRan2020 to 2023Enrolled70ConditionsSystemic Sclerosis, SclerodermaArmsPET-MRI scan
3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 25 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Systemic Sclerosis and Pulmonary Disease.Advances in experimental medicine and biology · 2021
    Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. 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

3 authors at 1 institution in 1 country.

Michael E JohnsonDepartment of Genetics, Geisel School of Medicine at Dartmouth, 7400 Remsen, Hanover, NH, 03755, USA.
Patricia A Pioli
Michael L Whitfield
Dartmouth College · US

Funding

Translational Engineering in Cancer (TEC)P30CA023108 · NCI · DARTMOUTH COLLEGE · PI Steven D Leach · 1985 to 2026
$91.3M
Translational studies for identifying and targeting novel pathways in systemic sclerosis pathogenesisP50AR060780 · NIAMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI LAFYATIS, ROBERT A. · 2011 to 2021
$14.9M
NCI NIH HHS P30 CA023108NIAMS NIH HHS P50 AR060780
6 · The paper itself

Abstract

Systemic sclerosis (SSc) is characterized by inflammation, vascular dysfunction, and ultimately fibrosis. Progress in understanding disease pathogenesis and developing effective disease treatments has been hampered by an incomplete understanding of SSc heterogeneity. To clarify this, we have used genomic approaches to identify distinct patient subsets based on gene expression patterns in SSc skin and other end-target organs. Here, we review what is known about the gene expression-based subsets in SSc, currently defined as the inflammatory, fibroproliferative, limited, and normal-like subsets. The inflammatory subset of patients is characterized by infiltrating immune cells that include T cells, macrophages, and possibly dendritic cells, although little is known about the mediators these cells secrete and the pathways that govern cell activation. Prior studies have suggested a role for pathogens as a trigger of immune responses in SSc, and recent data have identified viral and mycobiome components as potential environmental triggers. We present a model based on analyses of gene expression data and a review of the literature, which suggests that the gene expression subsets observed in patients possibly represent distinct, interconnected molecular states of disease, to which an innate immune response is central that results in the generation of clinical disease.

Indexed as

Gene Expression ProfilingHumansImmunity, InnateInflammationScleroderma, SystemicSignal TransductionSkin

Identifiers

PMID26223504
PMCPMC4722533
OpenAlexW1037072360

What OpenQuestion holds

Textmetadata
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Read underepoch 390

Registered trials

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.