Evidence map›Paper›PMID 21389262›Full record

ArticleScience translational medicine2011

Dissecting the immune cell mayhem that drives lupus pathogenesis.

Joseph E Craft

Open access · greenAbstract readComment
In one paragraph

Article in Science translational medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.9field-weighted citation impact, top 7% 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

22 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
  2. Utilization of Biomarkers in Lupus Nephritis.Advances in chronic kidney disease · 2019
    Review
  3. Article
  4. Review
  5. Precision medicine in lupus nephritis: can biomarkers get us there?Translational research : the journal of laboratory and clinical medicine · 2018
    Review
  6. Article
  7. Re-Examining Neutrophil Participation in GN.Journal of the American Society of Nephrology : JASN · 2017
    Review
  8. Review
  9. Review
  10. Galectin-3 in autoimmunity and autoimmune diseases.Experimental biology and medicine (Maywood, N.J.) · 2015
    Review
  11. Suppression of systemic autoimmunity by the innate immune adaptor STING.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  12. Deorphanization of the human leukocyte tyrosine kinase (LTK) receptor by a signaling screen of the extracellular proteome.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Joseph E CraftSection of Rheumatology, Department of Internal Medicine, and Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA. joseph.craft@yale.edu
Yale University · US

Funding

Yale Rheumatic Diseases Research Core CenterP30AR053495 · NIAMS · YALE UNIVERSITY · PI CRAFT, JOSEPH EDGAR · 2007 to 2017
$7.0M
GENETIC ANALYSIS OF T CELLS IN LUPUSR01AR044076 · NIAMS · YALE UNIVERSITY · PI CRAFT, JOSEPH EDGAR · 1996 to 2010
$4.1M
MOLECULAR CHARACTERIZATION OF THE SNRNP POLYPEPTIDESR01AR040072 · NIAMS · YALE UNIVERSITY · PI Joseph Edgar Craft · 1990 to 2026
$2.5M
Dissecting the role for IL-15 in CD8+ T cell homeostasis in human lupusR01AI075157 · NIAID · YALE UNIVERSITY · PI CRAFT, JOSEPH EDGAR · 2008 to 2012
$2.0M
NIAID NIH HHS 5 R01 AI075157NIAID NIH HHS R01 AI075157NIAMS NIH HHS P30 AR053495NIAMS NIH HHS R01 AR040072NIAMS NIH HHS R01 AR044076NIAMS NIH HHS R01 AR40072NIAMS NIH HHS R01 AR44076
6 · The paper itself

Abstract

The autoimmune disease systemic lupus erythematosus (SLE) results from an inability of the immune system to discriminate between certain self-antigens and foreign ones. The most common treatment of SLE involves the use of immunosuppressive drugs to reduce inflammation, but these therapies have serious side effects. Three recent papers in Science Translational Medicine redirect focus on neutrophils, platelets, and interferon-α in the pathogenesis of SLE and reinforce the notion that researchers should seek to discover and devise combination therapies that target these processes.

Indexed as

AutoantibodiesBlood PlateletsHumansInterferon-alphaLupus Erythematosus, SystemicModels, ImmunologicalNeutrophilsPlatelet ActivationAutoantibodiesInterferon-alpha

Identifiers

PMID21389262
PMCPMC3694130
OpenAlexW1997963127

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.