Evidence map›Paper›PMID 25309533›Full record

ReviewFrontiers in immunology2014

Type I interferons in bacterial infections: taming of myeloid cells and possible implications for autoimmunity.

Emily M Eshleman, Laurel L Lenz

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

26 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Review
  3. Interferon-β regulates proresolving lipids to promote the resolution of acute airway inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2022
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  10. Study of the immunogenicity ofIranian journal of basic medical sciences · 2019
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  13. Review
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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

2 authors at 1 institution in 1 country.

Emily M EshlemanDepartment of Immunology and Microbiology, University of Colorado School of Medicine , Aurora, CO , USA.
Laurel L LenzDepartment of Immunology and Microbiology, University of Colorado School of Medicine , Aurora, CO , USA ; Department of Biomedical Research, National Jewish Health , Denver, CO , USA.
University of Colorado Denver · US

Funding

Immune Modulation by Bacterial AutolysinsR01AI065638 · NIAID · UNIVERSITY OF COLORADO DENVER · PI LENZ, LAUREL L · 2006 to 2016
$3.8M
Molecular Pathogenesis of Infectious DiseasesT32AI052066 · NIAID · UNIVERSITY OF COLORADO DENVER · PI VAN DYK, LINDA F. · 2002 to 2022
$2.3M
IFNGR Down Regulation as a Host Target for Therapy of Infectious DiseasesR33AI102264 · NIAID · UNIVERSITY OF COLORADO DENVER · PI LENZ, LAUREL L · 2014 to 2016
$1.1M
IFNGR Down Regulation as a Host Target for Therapy of Infectious DiseasesR21AI102264 · NIAID · NATIONAL JEWISH HEALTH · PI LENZ, LAUREL L · 2012 to 2013
$436k
Non-canonical responses to IFNab in the suppression of macrophage immunityR21AI103782 · NIAID · UNIVERSITY OF COLORADO DENVER · PI LENZ, LAUREL L · 2013 to 2014
$432k
Active Subversion of Innate Immunity by Bacterial LysM ProteinR56AI065638 · NIAID · NATIONAL JEWISH HEALTH · PI LENZ, LAUREL L · 2011 to 2011
$396k
NIAID NIH HHS R01 AI065638NIAID NIH HHS R21 AI102264NIAID NIH HHS R21 AI103782NIAID NIH HHS R33 AI102264NIAID NIH HHS R56 AI065638NIAID NIH HHS T32 AI052066
6 · The paper itself

Abstract

Type I interferons (IFNs) were first described for their ability to protect the host from viral infections and may also have beneficial effects under specific conditions within some bacterial infections. Yet, these pleiotropic cytokines are now known to exacerbate infections by numerous life-threatening bacteria, including the intracellular pathogens Listeria monocytogenes and Mycobacterium tuberculosis. The evidence that such detrimental effects occur during bacterial infections in both animals and humans argues for selective pressure. In this review, we summarize the evidence demonstrating a pro-bacterial role for type I IFNs and discuss possible mechanisms that have been proposed to explain such effects. The theme emerges that type I IFNs act to suppress myeloid cell immune responses. The evolutionary conservation of such anti-inflammatory effects, particularly in the context of infections, suggests they may be important for limiting chronic inflammation. Given the effectiveness of type I IFNs in treatment of certain autoimmune diseases, their production may also act to raise the threshold for activation of immune responses to self-antigens.

Indexed as

autoimmunitybacterial pathogensimmune suppressioninterferon receptorsinterferonsmacrophage activation

Identifiers

PMID25309533
PMCPMC4161047
OpenAlexW2001191847

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.