Evidence map›Paper›PMID 21923413›Full record

ReviewJournal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research2011

Interferon alpha as a primary pathogenic factor in human lupus.

Timothy B Niewold

Abstract readReview
In one paragraph

Review in Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
97citing papers in PubMed, 1 pooled it
11.8field-weighted citation impact, top 1% 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

97 citing papers in PubMed, 1 synthesis or guideline pooled it, 150 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Observational
  6. Review
  7. Review
  8. Observational
  9. Analysis of Key Genes Related to Systemic Lupus Erythematosus and COVID-19.Combinatorial chemistry & high throughput screening · 2025
    Article
  10. Review
  11. Occurrence and role of Tph cells in various renal diseases.Molecular medicine (Cambridge, Mass.) · 2024
    Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review

37 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

Timothy B NiewoldSection of Rheumatology, Gwen Knapp Center for Lupus and Immunology Research, University of Chicago, Chicago, Illinois 60637, USA. tniewold@medicine.bsd.uchicago.edu
University of Chicago · US

Funding

ULTRASTRUCTURE AND CYTOMORPHOLOGY COREP30DK042086 · NIDDK · UNIVERSITY OF CHICAGO · PI ABADIE, VALERIE · 1990 to 2025
$29.8M
TRANSLATIONAL RESEARCH UNIVERSITY OF CHICAGO: CLINICAL TRIALSUL1RR024999 · NCRR · UNIVERSITY OF CHICAGO · PI SOLWAY, JULIAN · 2007 to 2011
$25.3M
Genetic Regulation of interferon Alpha in Human LupusK08AI083790 · NIAID · UNIVERSITY OF CHICAGO · PI NIEWOLD, TIMOTHY B · 2009 to 2013
$616k
NCRR NIH HHS UL1 RR024999NIAID NIH HHS AI071651NIAID NIH HHS K08 AI083790NIDDK NIH HHS P30 DK42086
6 · The paper itself

Abstract

Interferon alpha (IFN-α) is a critical mediator of human systemic lupus erythematosus (SLE). This review will summarize evidence supporting the role for IFN-α in the initiation of human SLE. IFN-α functions in viral immunity at the interface of innate and adaptive immunity, a position well suited to setting thresholds for autoimmunity. Some individuals treated with IFN-α for chronic viral infections develop de novo SLE, which frequently resolves when IFN-α is withdrawn, supporting the idea that IFN-α was causal. Abnormally high IFN-α levels are clustered within SLE families, suggesting that high serum IFN-α is a heritable risk factor for SLE. Additionally, SLE-risk genetic variants in the IFN-α pathway are gain of function in nature, resulting in either higher circulating IFN-α levels or greater sensitivity to IFN-α signaling in SLE patients. A recent genome-wide association study has identified additional novel genetic loci associated with high serum IFN-α in SLE patients. These data support the idea that genetically determined endogenous elevations in IFN-α predispose to human SLE. It is possible that some of these gain-of-function polymorphisms in the IFN-α pathway are useful in viral defense, and that risk of SLE is a burden we have taken on in the fight to defend ourselves against viral infection.

Indexed as

Genetic Predisposition to DiseaseHumansInterferon-alphaInterferon Regulatory FactorsLupus Erythematosus, SystemicModels, ImmunologicalPolymorphism, GeneticReceptors, ImmunologicSignal TransductionVirus DiseasesInterferon-alphaInterferon Regulatory FactorsReceptors, Immunologic

Identifiers

PMID21923413
PMCPMC3234490
OpenAlexW2048537061

What OpenQuestion holds

Textmetadata
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.