Evidence map›Paper›PMID 34138758›Full record

ArticleJCI insight2021

STAT4 is expressed in neutrophils and promotes antimicrobial immunity.

Pegah Mehrpouya-Bahrami, Alina K Moriarty, Paulo De Melo, W Coles Keeter, Nada S Alakhras, Andrew S Nelson, Madeline Hoover, Maria S Barrios, Jerry L Nadler, C Henrique Serezani and 2 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 2 pooled it
2.5field-weighted citation impact, top 10% 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, 2 syntheses or guidelines pooled it, 37 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. STAT4-dependent regulation of neuroinflammation in atherosclerosis.bioRxiv : the preprint server for biology · 2026
    Article
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  10. Review
  11. Investigating the Link betweenInternational journal of molecular sciences · 2024
    Article
  12. An IL-23-STAT4 pathway is required for the proinflammatory function of classical dendritic cells during CNS inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  13. STAT4 gene polymorphisms in human diseases.Frontiers in immunology · 2024
    Review
  14. Review
  15. Association ofBiomedicines · 2023
    Article
  16. Article
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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

12 authors at 4 institutions in 1 country.

Pegah Mehrpouya-BahramiDepartment of Microbiology and Immunology and.
Alina K MoriartyDepartment of Microbiology and Molecular Cell Biology, Eastern Virginia Medical School, Norfolk, Virginia, USA.
Paulo De MeloDivision of Infectious Diseases, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
W Coles KeeterDepartment of Microbiology and Molecular Cell Biology, Eastern Virginia Medical School, Norfolk, Virginia, USA.
Nada S AlakhrasDepartment of Biochemistry and Molecular Biology, School of Medicine, Indiana University, Indianapolis, Indiana, USA.
Andrew S NelsonDepartment of Microbiology and Immunology and.
Madeline HooverHerman B Wells Center for Pediatric Research, Department of Pediatrics, School of Medicine, Indiana University, Indianapolis, Indiana, USA.
Maria S BarriosHerman B Wells Center for Pediatric Research, Department of Pediatrics, School of Medicine, Indiana University, Indianapolis, Indiana, USA.
Jerry L NadlerDepartments of Medicine and Pharmacology, School of Medicine, New York Medical College, Valhalla, New York, USA.
C Henrique SerezaniDivision of Infectious Diseases, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Mark H KaplanDepartment of Microbiology and Immunology and.
Elena V GalkinaDepartment of Microbiology and Molecular Cell Biology, Eastern Virginia Medical School, Norfolk, Virginia, USA.
Indiana University – Purdue University Indianapolis · USEastern Virginia Medical School · USVanderbilt University Medical Center · USNew York Medical College · US

Funding

Tumor Microenvironment and Metastasis ProgramP30CA082709 · NCI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI Sara K Quinney · 1999 to 2026
$59.3M
Indiana Clinical and Translational Sciences InstituteUL1TR001108 · NCATS · INDIANA UNIVERSITY INDIANAPOLIS · PI DENNE, SCOTT C., SHEKHAR, ANANTHA · 2013 to 2017
$23.3M
Project-005U54DK106846 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI Reuben Kapur, Karen Elizabeth Pollok · 2015 to 2026
$9.7M
BASIC SCIENCE STUDIES ON GENE THERAPY OF BLOOD DISEASEST32HL007910 · NHLBI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI Roland W. Herzog, Reuben Kapur · 1999 to 2026
$7.6M
REGULATION OF HEMATOPOIETIC CELL PRODUCTIONT32DK007519 · NIDDK · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI KAPLAN, MARK H · 1986 to 2020
$7.1M
Validation of small molecule 12-lipoxygenase inhibitors in metabolic diseaseR01DK105588 · NIDDK · UNIVERSITY OF CHICAGO · PI KULKARNI, ROHIT N., MIRMIRA, RAGHAVENDRA G · 2015 to 2024
$5.5M
Phosphatase and tensin homolog PTEN actions in polymicrobial sepsisR01HL124159 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI SEREZANI, C. HENRIQUE · 2014 to 2022
$4.2M
Myeloid cell-specific role of STAT4 in atherosclerosis and metabolic dysfunctionR01HL142129 · NHLBI · EASTERN VIRGINIA MEDICAL SCHOOL · PI GALKINA, ELENA V, NADLER, JERRY L. · 2018 to 2021
$2.1M
Prostaglandin E2 Actions and Enhanced Susceptibility to Skin Infection in Diabetic MiceR01DK122147 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI SEREZANI, C. HENRIQUE · 2020 to 2022
$1.7M
Mechanisms underlying poor skin host defense in diabetic conditionsR21AI149207 · NIAID · VANDERBILT UNIVERSITY MEDICAL CENTER · PI SEREZANI, C. HENRIQUE · 2020 to 2021
$467k
NCATS NIH HHS UL1 TR001108NCI NIH HHS P30 CA082709NHLBI NIH HHS R01 HL124159NHLBI NIH HHS R01 HL142129NHLBI NIH HHS T32 HL007910NIAID NIH HHS R21 AI149207NIDDK NIH HHS R01 DK105588NIDDK NIH HHS R01 DK122147NIDDK NIH HHS T32 DK007519NIDDK NIH HHS U54 DK106846
6 · The paper itself

Abstract

Signal transducer and activator of transcription 4 (STAT4) is expressed in hematopoietic cells and plays a key role in the differentiation of T helper 1 cells. Although STAT4 is required for immunity to intracellular pathogens, the T cell-independent protective mechanisms of STAT4 are not clearly defined. In this report, we demonstrate that STAT4-deficient mice were acutely sensitive to methicillin-resistant Staphylococcus aureus (MRSA) infection. We show that STAT4 was expressed in neutrophils and activated by IL-12 via a JAK2-dependent pathway. We demonstrate that STAT4 was required for multiple neutrophil functions, including IL-12-induced ROS production, chemotaxis, and production of the neutrophil extracellular traps. Importantly, myeloid-specific and neutrophil-specific deletion of STAT4 resulted in enhanced susceptibility to MRSA, demonstrating the key role of STAT4 in the in vivo function of these cells. Thus, these studies identify STAT4 as an essential regulator of neutrophil functions and a component of innate immune responses in vivo.

Indexed as

AnimalsDisease Models, AnimalHumansImmunity, InnateInterleukin-12Janus Kinase 2MAP Kinase Signaling SystemMethicillin-Resistant Staphylococcus aureusMiceMice, KnockoutNeutrophilsStaphylococcal InfectionsSTAT4 Transcription FactorInterleukin-12Jak2 protein, mouseJanus Kinase 2Stat4 protein, mouseSTAT4 Transcription FactorImmunologyNeutrophils

Identifiers

PMID34138758
PMCPMC8410094
OpenAlexW3167458408

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.