Evidence map›Paper›PMID 21705616›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2011

IFN-α confers resistance of systemic lupus erythematosus nephritis to therapy in NZB/W F1 mice.

Zheng Liu, Ramalingam Bethunaickan, Weiqing Huang, Meera Ramanujam, Michael P Madaio, Anne Davidson

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

36 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Interferons in Systemic Lupus Erythematosus.Rheumatic diseases clinics of North America · 2021
    Review
  11. Punicalagin Ameliorates Lupus Nephritis via Inhibition of PAR2.International journal of molecular sciences · 2020
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. An update on lupus animal models.Current opinion in rheumatology · 2017
    Review
  19. Article
  20. Re-Examining Neutrophil Participation in GN.Journal of the American Society of Nephrology : JASN · 2017
    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

6 authors at 2 institutions in 1 country.

Zheng LiuCenter for Autoimmunity and Musculoskeletal Diseases, Feinstein Institute for Medical Research, Manhasset, New York, NY 11030, USA.
Ramalingam Bethunaickan
Weiqing Huang
Meera Ramanujam
Michael P Madaio
Anne Davidson
Feinstein Institute for Medical Research · USAugusta University · US

Funding

Targeting renal inflammatory pathways of SLE nephritis in mouse and manR01DK085241 · NIDDK · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI DAVIDSON, ANNE · 2010 to 2013
$2.2M
Regulation of the anti-phospholipid response in SLER01AI083901 · NIAID · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI DAVIDSON, ANNE · 2010 to 2014
$2.2M
Interferon Regulation in Systemic LupusR01AI059636 · NIAID · HOSPITAL FOR SPECIAL SURGERY · PI IVASHKIV, LIONEL B · 2006 to 2010
$2.0M
NIAID NIH HHS R01 AI059636NIAID NIH HHS R01 AI059636-01A2NIAID NIH HHS R01 AI083901NIDDK NIH HHS R01 DK085241
6 · The paper itself

Abstract

The critical role of IFN-α in the pathogenesis of human systemic lupus erythematosus has been highlighted in recent years. Exposure of young lupus-prone NZB/W F1 mice to IFN-α in vivo leads to an accelerated lupus phenotype that is dependent on T cells and is associated with elevated serum levels of BAFF, IL-6, and TNF-α, increased splenic expression of IL-6 and IL-21, formation of large germinal centers, and the generation of large numbers of short-lived plasma cells that produce IgG2a and IgG3 autoantibodies. In this study, we show that both IgG2a and IgG3 autoantibodies are pathogenic in IFN-α-accelerated lupus, and their production can be dissociated by using low-dose CTLA4-Ig. Only high-dose CTLA4-Ig attenuates both IgG2a and IgG3 autoantibody production and significantly delays death from lupus nephritis. In contrast, BAFF/APRIL blockade has no effect on germinal centers or the production of IgG anti-dsDNA Abs but, if given at the time of IFN-α challenge, delays the progression of lupus by attenuating systemic and renal inflammation. Temporary remission of nephritis induced by combination therapy with cyclophosphamide, anti-CD40L Ab, and CTLA4-Ig is associated with the abrogation of germinal centers and depletion of short-lived plasma cells, but relapse occurs more rapidly than in conventional NZB/W F1 mice. This study demonstrates that IFN-α renders NZB/W F1 relatively resistant to therapeutic intervention and suggests that the IFN signature should be considered when randomizing patients into groups and analyzing the results of human clinical trials in systemic lupus erythematosus.

Indexed as

Crosses, GeneticAbataceptAdenoviridaeAnimalsAutoantibodiesB-Cell Activating FactorDose-Response Relationship, DrugDrug Therapy, CombinationFemaleImmunity, InnateImmunoconjugatesInterferon-alphaLac OperonLupus Erythematosus, SystemicLupus NephritisMiceAbataceptAutoantibodiesB-Cell Activating FactorIfna1 protein, mouseImmunoconjugatesInterferon-alphaRecombinant Fusion ProteinsTACI receptor-IgG Fc fragment fusion proteinTnfsf13b protein, mouse

Identifiers

PMID21705616
PMCPMC3140572
OpenAlexW2108207992

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.