Evidence map›Paper›PMID 27274010›Full record

ArticleArthritis & rheumatology (Hoboken, N.J.)2016

A Novel Mechanism for Generating the Interferon Signature in Lupus: Opsonization of Dead Cells by Complement and IgM.

Haoyang Zhuang, Shuhong Han, Yi Li, Deborah Kienhöfer, Pui Lee, Stepan Shumyak, Richard Meyerholz, Krzysztof Rosadzinski, Danielle Rosner, Annie Chan and 6 more

Open access · greenAbstract read
In one paragraph

Article in Arthritis & rheumatology (Hoboken, N.J.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. A Novel Subset of Anti-Inflammatory CD138Journal of immunology (Baltimore, Md. : 1950) · 2017
    Article
  10. Pathogenesis of Diffuse Alveolar Hemorrhage in Murine Lupus.Arthritis & rheumatology (Hoboken, N.J.) · 2017
    Article
  11. Review
  12. Review
  13. 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

16 authors at 3 institutions in 2 countries.

Haoyang ZhuangUniversity of Florida, Gainesville.
Shuhong HanUniversity of Florida, Gainesville.
Yi LiUniversity of Florida, Gainesville.
Deborah KienhöferUniversitätsklinikum Erlangen, Erlangen, Germany.
Pui LeeBoston Children's Hospital, Boston, Massachusetts.
Stepan ShumyakUniversity of Florida, Gainesville.
Richard MeyerholzUniversity of Florida, Gainesville.
Krzysztof RosadzinskiUniversity of Florida, Gainesville.
Danielle RosnerUniversity of Florida, Gainesville.
Annie ChanUniversity of Florida, Gainesville.
Yuan XuUniversity of Florida, Gainesville.
Mark SegalUniversity of Florida, Gainesville.
Eric SobelUniversity of Florida, Gainesville.
Li-Jun YangUniversity of Florida, Gainesville.
Markus H HoffmannUniversitätsklinikum Erlangen, Erlangen, Germany.
Westley H ReevesUniversity of Florida, Gainesville.
University of Florida · USUniversitätsklinikum Erlangen · DEBoston Children's Hospital · US

Funding

Pathogenesis on Autoantibodies in Pristane-Induced LupusR01AR044731 · NIAMS · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI REEVES, WESTLEY H · 1997 to 2021
$6.6M
NIAMS NIH HHS R01 AR044731
6 · The paper itself

Abstract

objectiveIn vitro studies suggest that the type I interferon (IFN) signature seen in most lupus patients results from Fcγ receptor-mediated uptake of nucleic acid-containing immune complexes by plasmacytoid dendritic cells and engagement of endosomal Toll-like receptors. The aim of this study was to reexamine the pathogenesis of the IFN signature in vivo.

methodsLupus was induced in mice by injecting pristane. Some mice were treated with normal immunoglobulin or with cobra venom factor to deplete complement. The IFN signature was evaluated by polymerase chain reaction. The IFN signature also was determined in C4-deficient patients and control subjects.

resultsWild-type C57BL/6 mice with pristane-induced lupus developed a strong IFN signature, which was absent in immunoglobulin-deficient (μMT), C3

conclusionThese studies define previously unrecognized roles of natural IgM, complement, and complement receptors in generating the IFN signature in lupus.

Indexed as

AdultAnimalsApoptosisAutoantibodiesCase-Control StudiesCD18 AntigensComplement C3Complement C4Complement Inactivating AgentsComplement System ProteinsCytokinesDisease Models, AnimalElapid VenomsEnzyme-Linked Immunosorbent AssayFemaleFlow CytometryAutoantibodiesCD18 Antigenscobra venom factorComplement C3Complement C4Complement Inactivating AgentsComplement System ProteinsCytokinesElapid VenomsImmunoglobulin GImmunoglobulin MImmunosuppressive AgentsInterferon Type IOpsonin ProteinspristaneTerpenes

Identifiers

PMID27274010
PMCPMC5125898
OpenAlexW2409777419

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.