Evidence map›Paper›PMID 40180328›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2025

Cutting Edge: Cooperative interferon regulatory factor network shapes the NK-cell antiviral response.

Endi K Santosa, Jennifer M Zhang, John C Sauter, Mark Owyong, Joseph C Sun

Abstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

5 authors.

Endi K SantosaImmunology Program, Memorial Sloan Kettering Cancer Center, New York, NY, United States.ORCID 0000-0001-9483-8354
Jennifer M ZhangImmunology Program, Memorial Sloan Kettering Cancer Center, New York, NY, United States.ORCID 0009-0003-1985-2967
John C SauterImmunology Program, Memorial Sloan Kettering Cancer Center, New York, NY, United States.ORCID 0009-0008-8104-4844
Mark OwyongImmunology Program, Memorial Sloan Kettering Cancer Center, New York, NY, United States.
Joseph C SunImmunology Program, Memorial Sloan Kettering Cancer Center, New York, NY, United States.ORCID 0000-0001-8062-9033

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Hongbiao Carl Lekaye · 1985 to 2026
$347.4M
The natural killer cell response against mouse cytomegalovirus infectionR01AI100874 · NIAID · SLOAN-KETTERING INST CAN RESEARCH · PI Joseph Chai-Yuen Sun · 2012 to 2026
$7.4M
Transcriptional control of NK cell metabolismR01AI155558 · NIAID · SLOAN-KETTERING INST CAN RESEARCH · PI Joseph Chai-Yuen Sun · 2021 to 2026
$4.7M
Regulation of Nfil3 in innate lymphocyte-mediated host immunityR01AI130043 · NIAID · SLOAN-KETTERING INST CAN RESEARCH · PI SUN, JOSEPH CHAI-YUEN · 2017 to 2021
$2.8M
Role of Frizzled 5 in NK cell development and antiviral host immunityF31AI178958 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI Mark Owyong · 2023 to 2026
$147k
American Cancer SocietyBurroughs Wellcome FundLudwig Center for Cancer ImmunotherapyNational Institute of Health AI100874National Institute of Health AI130043National Institute of Health AI155558National Institute of Health P30CA008748NCI NIH HHS P30 CA008748NIAID NIH HHS F31 AI178958NIAID NIH HHS R01 AI100874NIAID NIH HHS R01 AI130043NIAID NIH HHS R01 AI155558
6 · The paper itself

Abstract

Natural killer (NK) cells are innate lymphocytes that exhibit adaptive traits particularly evident during cytomegalovirus (CMV) infection. Following mouse CMV (MCMV) infection, NK cells upregulate the transcription factors IRF4 and IRF8, which are indispensable for their survival and proliferation upon viral infection. However, it is unclear whether these factors are expressed within the same individual cell and whether deficiency in one could be compensated by the other. In this study, we observed that a subset of NK cells co-express high levels of IRF4 and IRF8 in an NFκB-dependent manner. These IRF4HighIRF8High NK cells are specifically enriched for activated but immature cells with high proliferative potential during MCMV infection. Functionally, NK cells lacking both IRF4 and IRF8 develop normally, but experience a more severe expansion defect during virus exposure compared to NK cells deficient in a single factor. Thus, our study reveals a cooperative interplay between IRF4- and IRF8-dependent transcriptional networks in regulating NK-cell antiviral responses.

Indexed as

Herpesviridae InfectionsInterferon Regulatory FactorsKiller Cells, NaturalMuromegalovirusAnimalsGene Regulatory NetworksImmunity, InnateInterferon Regulatory Factor-4Interferon Regulatory Factor-8MiceMice, Inbred C57BLMice, KnockoutNF-kappa BInterferon Regulatory Factor-4Interferon Regulatory Factor-8Interferon Regulatory FactorsNF-kappa BInnate immunityinterferon regulatory factornatural killer cellstranscriptional regulationviral infection

Identifiers

PMID40180328
PMCPMC12213180

What Socratic 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 Socratic graph.