Evidence map›Paper›PMID 41290006›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2026

Aging changes the mechanism that underlies JAK2 modulation of neutrophil function.

Jacob W Feldmann, Matthew Kays, Farrah McGinnis, Emily Herron, Nurullah Sati, Clara Woods, Aminata P Coulibaly

Abstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2026. 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

7 authors.

Jacob W FeldmannDepartment of Neuroscience, Rockefeller Neuroscience Institute, West Virginia University, Morgantown, WV, United States.
Matthew KaysDepartment of Neuroscience, Rockefeller Neuroscience Institute, West Virginia University, Morgantown, WV, United States.
Farrah McGinnisDepartment of Neuroscience, Rockefeller Neuroscience Institute, West Virginia University, Morgantown, WV, United States.
Emily HerronDepartment of Neuroscience, Rockefeller Neuroscience Institute, West Virginia University, Morgantown, WV, United States.
Nurullah SatiDepartment of Neuroscience, Rockefeller Neuroscience Institute, West Virginia University, Morgantown, WV, United States.
Clara WoodsDepartment of Neuroscience, Rockefeller Neuroscience Institute, West Virginia University, Morgantown, WV, United States.
Aminata P CoulibalyDepartment of Neuroscience, Rockefeller Neuroscience Institute, West Virginia University, Morgantown, WV, United States.ORCID 0000-0002-9184-895X

Funding

WVU Flow Cytometry and Single Cell Core Facility (FCSCCF)P20GM121322 · NIGMS · WEST VIRGINIA UNIVERSITY · PI Paul R Lockman · 2018 to 2026
$22.4M
Defining the role of meningeal neutrophils in cognitionK22NS114363 · NINDS · WEST VIRGINIA UNIVERSITY · PI COULIBALY, AMINATA PORHY · 2020 to 2024
$859k
Special Becton Dickinson Fortessa Flow CytometerS10OD016165 · OD · WEST VIRGINIA UNIVERSITY · PI CUFF, CHRISTOPHER F · 2013 to 2013
$384k
National Institute of Health Office of the DirectorNIGMS NIH HHSNIGMS NIH HHS P20 GM121322NIH HHS S10 OD016165NINDS NIH HHSNINDS NIH HHS K22 NS114363
6 · The paper itself

Abstract

Janus kinase 2 (JAK2) has been linked to various neutrophil functions, but the intracellular mechanisms underlying its modulation are unknown. Neutrophils are essential cells for host defense. Neutrophil effector functions include migration, neutrophil extracellular trap production (NETosis), reactive oxygen species (ROS) production, and degranulation. The goal of this study was to elucidate the signaling mechanism through which JAK2 modulates neutrophil function and the effect of aging on this pathway. We hypothesized that JAK2-mediated modulation changes the molecular mechanisms associated with neutrophil function in an age-dependent manner. Neutrophils from young (3 mo) and aged (≥22 mo) male and female C57BL/6J mice were isolated, treated with a JAK2 inhibitor (AZD1480) or a pan-JAK inhibitor (baricitinib), and stimulated with PMA. Functional assays were conducted to assess migration, degranulation, NETosis, and metabolism. Mass spectrometry and Luminex assays provided proteomic and cytokine profiles. Our data showed that JAK2 promotes migration via membrane composition and actin remodeling, with age-dependent shifts in chemokine secretion. JAK2 primes ROS production by altering NADPH oxidase components, which contributes to NET production. JAK2 influences degranulation through actin remodeling. While aged neutrophils display impaired ROS-granule release, both young and aged neutrophils have distinct JAK-dependent release of granule contents. Metabolically, JAK2 enhances pentose phosphate pathway activity in young neutrophils and decreases glycogen breakdown in aged cells. These findings reveal mechanisms by which JAK2 modulates neutrophil function and suggest that organismal age plays a role in this modulation.

Indexed as

AgingJanus Kinase 2NeutrophilsAnimalsCell DegranulationCell MovementExtracellular TrapsFemaleMaleMiceMice, Inbred C57BLReactive Oxygen SpeciesSignal TransductionJak2 protein, mouseJanus Kinase 2Reactive Oxygen SpeciesdegranulationJAK2metabolismmigrationneutrophils

Identifiers

PMID41290006
PMCPMC12908130

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Registered trials

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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.