Evidence map›Paper›PMID 38417030›Full record

ArticleJournal of leukocyte biology2024

PTP1B phosphatase dampens iPSC-derived neutrophil motility and antimicrobial function.

Morgan A Giese, David A Bennin, Taylor J Schoen, Ashley N Peterson, Jonathan H Schrope, Josh Brand, Ho Sun Jung, Nancy P Keller, David J Beebe, Huy Q Dinh and 2 more

Open access · greenAbstract read
In one paragraph

Article in Journal of leukocyte biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

10 citing papers in PubMed, 8 citations in OpenAlex.

  1. CAR-engineered neutrophils derived from induced pluripotent stem cells: a new frontier in cellular immunotherapy.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 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

12 authors at 1 institution in 1 country.

Morgan A GieseDepartment of Medical Microbiology and Immunology, University of Wisconsin-Madison, 1550 Linden Dr. Madison 53706, WI, United States.
David A BenninDepartment of Medical Microbiology and Immunology, University of Wisconsin-Madison, 1550 Linden Dr. Madison 53706, WI, United States.
Taylor J SchoenDepartment of Medical Microbiology and Immunology, University of Wisconsin-Madison, 1550 Linden Dr. Madison 53706, WI, United States.
Ashley N PetersonDepartment of Medical Microbiology and Immunology, University of Wisconsin-Madison, 1550 Linden Dr. Madison 53706, WI, United States.
Jonathan H SchropeDepartment of Biomedical Engineering, University of Wisconsin-Madison, 1550 Engineering Dr. Madison 53706, WI, United States.
Josh BrandCell and Molecular Pathology Graduate Program, University of Wisconsin-Madison, 1685 Highland Ave. Madison 53705, WI, United States.
Ho Sun JungWisconsin National Primate Research Center, University of Wisconsin-Madison, 1223 Capitol Ct. Madison 53715, WI, United States.
Nancy P KellerDepartment of Medical Microbiology and Immunology, University of Wisconsin-Madison, 1550 Linden Dr. Madison 53706, WI, United States.
David J BeebeCarbone Cancer Center, University of Wisconsin-Madison, 1111 Highland Ave. Madison 53705, WI, United States.
Huy Q DinhDepartment of Oncology, McArdle Laboratory for Cancer Research, School of Medicine and Public Health, University of Wisconsin-Madison, 1111 Highland Ave. Madison 53705, WI, United States.
Igor I SlukvinWisconsin National Primate Research Center, University of Wisconsin-Madison, 1223 Capitol Ct. Madison 53715, WI, United States.
Anna HuttenlocherDepartment of Medical Microbiology and Immunology, University of Wisconsin-Madison, 1550 Linden Dr. Madison 53706, WI, United States.ORCID 0000-0001-7940-6254
University of Wisconsin–Madison · US

Funding

Biotechnology Training ProgramT32GM135066 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI SCOTT M. COYLE, BRIAN G FOX · 2020 to 2026
$7.0M
Microbial Pathogenesis &Host Responses Training ProgramT32AI055397 · NIAID · UNIVERSITY OF WISCONSIN-MADISON · PI KLEIN, BRUCE STEVEN · 2003 to 2024
$5.5M
Microscale models of inflammation and its resolutionR01AI134749 · NIAID · UNIVERSITY OF WISCONSIN-MADISON · PI BEEBE, DAVID J, HUTTENLOCHER, ANNA · 2018 to 2022
$3.8M
National Institute of Allergy and Infectious DiseasesNIAID NIH HHS R01 AI134749NIAID NIH HHS T32 AI055397NIGMS NIH HHS T32 GM135066NIH HHS RO1 AI134749-05
6 · The paper itself

Abstract

Neutrophils are rapidly recruited to sites of infection and are critical for pathogen clearance. Therapeutic use of primary neutrophils has been limited, as they have a short lifespan and are not amenable to genetic manipulation. Human induced pluripotent stem cells (iPSCs) can provide a robust source of neutrophils for infusion and are genetically tractable. However, current work has indicated that dampened intracellular signaling limits iPSC-derived neutrophil (iNeutrophil) cellular activation and antimicrobial response. Here, we show that protein tyrosine phosphatase 1B (PTP1B) inhibits intracellular signaling and dampens iNeutrophil effector function. Deletion of the PTP1B phosphatase increased PI3K and ERK signaling and was associated with increased F-actin polymerization, cell migration, and phagocytosis. In contrast, other effector functions like NETosis and reactive oxygen species production were reduced. PTP1B-deficient neutrophils were more responsive to Aspergillus fumigatus and displayed rapid recruitment and control of hyphal growth. Accordingly, depletion of PTP1B increased production of inflammatory factors including the neutrophil chemokine interleukin-8. Taken together, these findings suggest that PTP1B limits iNeutrophil motility and antimicrobial function.

Indexed as

Cell MovementInduced Pluripotent Stem CellsNeutrophilsProtein Tyrosine Phosphatase, Non-Receptor Type 1ActinsAspergillus fumigatusExtracellular TrapsHumansPhagocytosisPhosphatidylinositol 3-KinasesReactive Oxygen SpeciesSignal TransductionActinsPhosphatidylinositol 3-KinasesProtein Tyrosine Phosphatase, Non-Receptor Type 1PTPN1 protein, humanReactive Oxygen Specieschemotaxisfungalneutrophilphosphatasestem cell

Identifiers

PMID38417030
PMCPMC11212797
OpenAlexW4392230172

What Socratic holds

Textmetadata
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.