Evidence map›Paper›PMID 22430248›Full record

ReviewImmunology and cell biology2012

Role of type I interferons in the activation of autoreactive B cells.

Kerstin Kiefer, Michael A Oropallo, Michael P Cancro, Ann Marshak-Rothstein

Abstract readReview
In one paragraph

Review in Immunology and cell biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 141 papers.

0numbers the graph read from it
0cells of the map it votes in
141citing papers in PubMed
7.9field-weighted citation impact, top 2% 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

141 citing papers in PubMed, 219 citations in OpenAlex.

  1. Trial
  2. InterferonFrontiers in immunology · 2020
    Trial
  3. Trial
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. NETosis: A key player in autoimmunity, COVID-19, and long COVID.Journal of translational autoimmunity · 2025
    Review
  16. BeyondInternational journal of molecular sciences · 2025
    Article
  17. Article
  18. Article
  19. Article
  20. Article

81 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

4 authors at 2 institutions in 1 country.

Kerstin KieferDepartment of Medicine, University of Massachusetts School of Medicine, Worcester, MA 01605, USA.
Michael A Oropallo
Michael P Cancro
Ann Marshak-Rothstein
University of Massachusetts Chan Medical School · USUniversity of Pennsylvania · US

Funding

Toll-Like Receptors in Systemic Autoimmune DiseaseP01AR050256 · NIAMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI SHLOMCHIK, MARK J · 2004 to 2013
$13.4M
B CELL HYPERACTIVITY IN AUTOIMMUNITYR01AR035230 · NIAMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI MARSHAK-ROTHSTEIN, ANN · 1986 to 2010
$3.2M
NIAMS NIH HHS P01 AR050256NIAMS NIH HHS R01 AR035230
6 · The paper itself

Abstract

Type I interferons (IFNs) are a family of cytokines involved in the defense against viral infections that play a key role in the activation of both the innate and adaptive immune system. IFNs both directly and indirectly enhance the capacity of B lymphocytes to respond to viral challenge and produce cytotoxic and neutralizing antibodies. However, prolonged type I IFN exposure is not always beneficial to the host. If not regulated properly IFN can drive autoantibody production as well as other parameters of systemic autoimmune disease. Type I IFNs impact B-cell function through a variety of mechanisms, including effects on receptor engagement, Toll-like receptor expression, cell migration, antigen presentation, cytokine responsiveness, cytokine production, survival, differentiation and class-switch recombination. Type I IFNs are also cytotoxic for a variety of cell types and thereby contribute to the accumulation of cell debris that serves as a potential source for autoantigens. Type I IFN engagement of a variety of accessory cells further promotes B-cell survival and activation, as exemplified by the capacity of type I IFNs to increase the level of B-cell survival factors, such as B lymphocyte stimulator, produced by dendritic cells. Therefore, it is not surprising that the loss of expression of the type I IFN receptor can have dramatic effects on the production of autoantibodies and on the clinical features of systemic autoimmune diseases such as systemic lupus erythematosus.

Indexed as

Lymphocyte ActivationAdaptive ImmunityAnimalsAutoimmune DiseasesAutoimmunityB-Cell Activating FactorB-LymphocytesCell SurvivalHumansImmunity, InnateInterferon Type IVirus DiseasesB-Cell Activating FactorInterferon Type I

Identifiers

PMID22430248
PMCPMC3701256
OpenAlexW1988458651

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.