Evidence map›Paper›PMID 38567833›Full record

ReviewImmunological reviews2024

Interferons and epigenetic mechanisms in training, priming and tolerance of monocytes and hematopoietic progenitors.

Bikash Mishra, Lionel B Ivashkiv

Open access · greenAbstract readReview
In one paragraph

Review in Immunological reviews, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
7.0field-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

25 citing papers in PubMed, 29 citations in OpenAlex.

  1. Monocytes in pneumonia: Functional plasticity and innate memory (Review).International journal of molecular medicine · 2026
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  15. The authors respond to feedback onFrontiers in oncology · 2026
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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.

Bikash MishraHSS Research Institute and David Z. Rosensweig Genomics Research Center, Hospital for Special Surgery, New York, New York, USA.
Lionel B IvashkivHSS Research Institute and David Z. Rosensweig Genomics Research Center, Hospital for Special Surgery, New York, New York, USA.ORCID 0000-0002-9951-0646
Hospital for Special Surgery · US

Funding

STEROID THERAPY AND CYTOKINES IN RHEUMATIC DISEASESR01AI046712 · NIAID · HOSPITAL FOR SPECIAL SURGERY · PI IVASHKIV, LIONEL B · 2000 to 2025
$12.5M
Inhibition of STAT3 and inflammatory cytokine productionR01AI044938 · NIAID · HOSPITAL FOR SPECIAL SURGERY · PI IVASHKIV, LIONEL B · 2000 to 2025
$9.2M
CYTOKINE REGULATION OF RA SYNOVIOCYTE PHENOTYPER01AR046713 · NIAMS · HOSPITAL FOR SPECIAL SURGERY · PI IVASHKIV, LIONEL B · 1999 to 2025
$8.3M
Fc Receptors &Cytokine Balance in Rheumatoid ArthritisR01AR050401 · NIAMS · HOSPITAL FOR SPECIAL SURGERY · PI Lionel B Ivashkiv · 2004 to 2026
$7.4M
Negative Regulation of OsteoclastogenesisR01DE019420 · NIDCR · HOSPITAL FOR SPECIAL SURGERY · PI IVASHKIV, LIONEL B · 2008 to 2022
$6.0M
HSS Research Institute Rheumatology TrainingT32AR071302 · NIAMS · HOSPITAL FOR SPECIAL SURGERY · PI ALESSANDRA B PERNIS, Jane E Salmon · 2017 to 2026
$2.3M
INHIBITION OF IL-6 AND STAT3 IN RHEUMATOID ARTHRITISR21AI044938 · NIAID · HOSPITAL FOR SPECIAL SURGERY · PI IVASHKIV, LIONEL B · 1999 to 1999
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National Institute of Allergy and Infectious Diseases AI044938National Institute of Allergy and Infectious Diseases AI046712NIAID NIH HHS R01 AI044938NIAID NIH HHS R01 AI046712NIAID NIH HHS R21 AI044938NIAMS NIH HHS AR046713NIAMS NIH HHS AR050401NIAMS NIH HHS R01 AR046713NIAMS NIH HHS R01 AR050401NIAMS NIH HHS T32 AR071302NIDCR NIH HHS DE019420NIDCR NIH HHS R01 DE019420
6 · The paper itself

Abstract

Training and priming of innate immune cells involve preconditioning by PAMPs, DAMPs, and/or cytokines that elicits stronger induction of inflammatory genes upon secondary challenge. Previous models distinguish training and priming based upon whether immune activation returns to baseline prior to secondary challenge. Tolerance is a protective mechanism whereby potent stimuli induce refractoriness to secondary challenge. Training and priming are important for innate memory responses that protect against infection, efficacy of vaccines, and maintaining innate immune cells in a state of readiness; tolerance prevents toxicity from excessive immune activation. Dysregulation of these processes can contribute to pathogenesis of autoimmune/inflammatory conditions, post-COVID-19 hyperinflammatory states, or sepsis-associated immunoparalysis. Training, priming, and tolerance regulate similar "signature" inflammatory genes such as TNF, IL6, and IL1B and utilize overlapping epigenetic mechanisms. We review how interferons (IFNs), best known for activating JAK-STAT signaling and interferon-stimulated genes, also play a key role in regulating training, priming, and tolerance via chromatin-mediated mechanisms. We present new data on how monocyte-to-macrophage differentiation modulates IFN-γ-mediated priming, affects regulation of AP-1 and CEBP activity, and attenuates superinduction of inflammatory genes. We present a "training-priming continuum" model that integrates IFN-mediated priming into current concepts about training and tolerance and proposes a central role for STAT1 and IRF1.

Indexed as

Epigenesis, GeneticHematopoietic Stem CellsImmune ToleranceInterferonsMonocytesAnimalsCell DifferentiationCOVID-19HumansImmunity, InnateImmunologic MemorySARS-CoV-2Signal TransductionInterferonschromatinepigeneticsinnate immune traininginterferonmonocytespriming

Identifiers

PMID38567833
PMCPMC11102283
OpenAlexW4393885149

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.