Evidence map›Paper›PMID 26276875›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2015

Cutting Edge: Hematopoietic Stem Cell Expansion and Common Lymphoid Progenitor Depletion Require Hematopoietic-Derived, Cell-Autonomous TLR4 in a Model of Chronic Endotoxin.

Ailing Liu, Yujuan Wang, Ying Ding, Ineavely Baez, Kimberly J Payne, Lisa Borghesi

Abstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

45 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
  2. Review
  3. Emergency myelopoiesis in solid cancers.British journal of haematology · 2024
    Review
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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

6 authors at 2 institutions in 2 countries.

Ailing LiuDepartment of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261;
Yujuan WangDepartment of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261;
Ying DingDepartment of Biostatistics, University of Pittsburgh Graduate School of Public Health, Pittsburgh, PA 15261; and.
Ineavely BaezDepartment of Pathology and Human Anatomy, Loma Linda University, Loma Linda, CA 92350.
Kimberly J PayneDepartment of Pathology and Human Anatomy, Loma Linda University, Loma Linda, CA 92350.
Lisa BorghesiDepartment of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261; borghesi@pitt.edu.
University of Pittsburgh · USLoma Linda University · US

Funding

VECTOR CORE FACILITYP30CA047904 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Jessie Nedrow · 1988 to 2026
$158.0M
NIH-LLU Initiative for Maximizing Student DiversityR25GM060507 · NIGMS · LOMA LINDA UNIVERSITY · PI DE LEON, MARINO · 2001 to 2022
$11.3M
Research Training/Education CoreP20MD006988 · NIMHD · LOMA LINDA UNIVERSITY · PI CASIANO, CARLOS A. · 2012 to 2016
$6.2M
The role of E47 in uncommitted hematopoietic progenitorsR01AI079047 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BORGHESI, LISA · 2009 to 2013
$1.6M
Mechanisms of TLR4-mediated impairment of murine and human HSC functionR21AI105846 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BORGHESI, LISA · 2014 to 2015
$431k
Special BD LSRFortessaTMS10OD011925 · OD · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BORGHESI, LISA · 2012 to 2012
$383k
Cellular and molecular mechanisms of HSC dysfunction in chronic inflammationR56AI079047 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BORGHESI, LISA · 2015 to 2015
$378k
NCI NIH HHS P30 CA047904NCI NIH HHS P30 CA4790413NIAID NIH HHS AI079047NIAID NIH HHS AI105846NIAID NIH HHS R01 AI079047NIAID NIH HHS R21 AI105846NIAID NIH HHS R56 AI079047NIGMS NIH HHS R25 GM060507NIH HHS S10 OD011925NIMHD NIH HHS P20 MD006988
6 · The paper itself

Abstract

Hematopoietic stem and progenitors cells (HSPCs) are activated through TLR4 in vitro. However, it remains unclear whether in vivo TLR4 sensing by HSPCs occurs directly or via other cell intermediates. In this study, we examined the cellular mechanisms underlying murine hematopoietic stem cell (HSC) expansion and common lymphoid progenitor (CLP) depletion in a model of chronic low-dose LPS. Using adoptive-transfer approaches, we show that HSC and CLP sensitivity to chronic LPS depends on hematopoietic-derived, cell subset-autonomous TLR4. Like murine progenitors, human HSPCs are activated by TLR4 in vitro. Using humanized mice, a preclinical model relevant to human physiology, we show that persistent endotoxin increases the frequency of Ki-67(+) HSCs and severely depletes CLPs and B precursors. Together, our findings show that murine HSPCs directly respond to endotoxin in vivo and that persistent LPS, a feature of several diseases of global health significance, impairs human lymphopoiesis.

Indexed as

Adoptive TransferAnimalsCell LineageCells, CulturedFetal BloodHematopoietic Stem CellsHematopoietic Stem Cell TransplantationHumansKi-67 AntigenLipopolysaccharidesLymphocyte DepletionLymphoid Progenitor CellsLymphopoiesisMiceMice, Inbred C57BLMice, Inbred NODKi-67 AntigenLipopolysaccharidesMki67 protein, mouseTlr4 protein, mouseToll-Like Receptor 4

Identifiers

PMID26276875
PMCPMC4561199
OpenAlexW1765297053

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.