Evidence map›Paper›PMID 26352734›Full record

ReviewCurrent opinion in rheumatology2015

Update on macrophages and innate immunity in scleroderma.

Jennifer J Chia, Theresa T Lu

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in rheumatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

21 citing papers in PubMed, 42 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Endothelial-to-mesenchymal transition in systemic sclerosis.Clinical and experimental immunology · 2021
    Review
  9. Review
  10. Article
  11. Observational
  12. Review
  13. Article
  14. Evolving insights into the cellular and molecular pathogenesis of fibrosis in systemic sclerosis.Translational research : the journal of laboratory and clinical medicine · 2019
    Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. 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

2 authors at 2 institutions in 1 country.

Jennifer J ChiaaWeill Cornell/Rockefeller/Sloan-Kettering Tri-Institutional MD-PhD Program bImmunology and Microbial Pathogenesis Program, Weill Cornell Graduate School of Medical Sciences cAutoimmunity and Inflammation Program dAutoimmunity and Inflammation Program and Department of Pediatric Rheumatology, Hospital for Special Surgery eDepartment of Microbiology and Immunology, Weill Cornell Medical College, New York, USA.
Theresa T Lu
Cornell University · USHospital for Special Surgery · US

Funding

Weill Cornell/Rockefeller/Sloan-Kettering MST ProgramT32GM007739 · NIGMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI HSU, KATHARINE C · 1985 to 2023
$51.1M
CTSA INFRASTRUCTURE FOR PEDIATRIC RESEARCHUL1RR024996 · NCRR · WEILL MEDICAL COLL OF CORNELL UNIV · PI IMPERATO-MCGINLEY, JULIANNE L · 2007 to 2011
$49.6M
Clinical and Translational Science CenterUL1TR000457 · NCATS · WEILL MEDICAL COLL OF CORNELL UNIV · PI IMPERATO-MCGINLEY, JULIANNE L · 2012 to 2016
$46.0M
Vascular-stromal function and regulation in immunityR01AI079178 · NIAID · HOSPITAL FOR SPECIAL SURGERY · PI Theresa T. Lu · 2010 to 2026
$6.6M
IMMUNOLOGY RESEARCH TRAINING PROGRAMT32AI007621 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI CESARMAN, ETHEL · 1999 to 2014
$3.4M
NCATS NIH HHS UL1 TR000457NCRR NIH HHS 5UL1RR024996NCRR NIH HHS UL1 RR024996NIAID NIH HHS R01 AI079178NIAID NIH HHS T32 AI007621NIAID NIH HHS T32AI007621NIGMS NIH HHS T32 GM007739NIGMS NIH HHS T32GM007739
6 · The paper itself

Abstract

purpose of reviewIn this review of the literature from 2014 through mid-2015, we examine new data that shed light on how macrophages and other innate immune cells and signals contribute to inflammation, vascular dysfunction, and fibrosis in scleroderma. RECENT

findingsRecent human studies have focused on changes early in scleroderma, and linked macrophages to inflammation in skin and progression of lung disease. Plasmacytoid dendritic cells have been implicated in vascular dysfunction. In mice, several factors have been identified that influence macrophage activation and experimental fibrosis. However, emerging data also suggest that myeloid cells can have differential effects in fibrosis. Sustained signaling through different toll-like receptors can lead to inflammation or fibrosis, and these signals can influence both immune and nonimmune cells. SUMMARY: There are many types of innate immune cells that can potentially contribute to scleroderma and will be worth exploring in detail. Experimentally dissecting the roles of macrophages based on ontogeny and activation state, and the innate signaling pathways in the tissue microenvironment, may also lead to better understanding of scleroderma pathogenesis.

Indexed as

Immunity, InnateAnimalsDendritic CellsFibrosisHumansInflammationMacrophagesMiceScleroderma, Systemic

Identifiers

PMID26352734
PMCPMC4763869
OpenAlexW2408394704

What OpenQuestion holds

Textmetadata
LicenceTDM
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.