Evidence map›Paper›PMID 20164424›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2010

A distinct subset of proinflammatory neutrophils isolated from patients with systemic lupus erythematosus induces vascular damage and synthesizes type I IFNs.

Michael F Denny, Srilakshmi Yalavarthi, Wenpu Zhao, Seth G Thacker, Marc Anderson, Ashley R Sandy, W Joseph McCune, Mariana J Kaplan

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 441 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
441citing papers in PubMed, 1 pooled it
13.5field-weighted citation impact, top 1% 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

441 citing papers in PubMed, 1 synthesis or guideline pooled it, 684 citations in OpenAlex.

  1. Pooled it
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  15. ROS Activated NETosis of Bone Marrow CD55Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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381 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Michael F DennyDivision of Rheumatology, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
Srilakshmi Yalavarthi
Wenpu Zhao
Seth G Thacker
Marc Anderson
Ashley R Sandy
W Joseph McCune
Mariana J Kaplan
Center for Rheumatology · USUniversity of Michigan · US

Funding

XenograftP30CA046592 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Scott Michael Schuetze · 1988 to 2026
$178.2M
MICHIGAN INSTITUTE FOR CLINICAL AND HEALTH RESEARCH (MICHR) (UL1): (BPCA)UL1RR024986 · NCRR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SHANLEY, THOMAS P. · 2007 to 2011
$51.2M
Vector CoreP30AR048310 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI FOX, DAVID A · 2001 to 2010
$5.9M
NETs in the development of lupus and its cardiovascular complicationsR01HL088419 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI EITZMAN, DANIEL T · 2009 to 2016
$3.1M
NCI NIH HHS P30 CA046592NCI NIH HHS P30CA46592NCRR NIH HHS UL1 RR024986NCRR NIH HHS UL1RR024986NHLBI NIH HHS HL088419NHLBI NIH HHS R01 HL088419NIAMS NIH HHS P30 AR048310NIAMS NIH HHS P30 AR48310
6 · The paper itself

Abstract

Neutrophil-specific genes are abundant in PBMC microarrays from lupus patients because of the presence of low-density granulocytes (LDGs) in mononuclear cell fractions. The functionality and pathogenicity of these LDGs have not been characterized. We developed a technique to purify LDGs from lupus PBMCs and assessed their phenotype, function, and potential role in disease pathogenesis. LDGs, their autologous lupus neutrophils, and healthy control neutrophils were compared with regard to their microbicidal and phagocytic capacities, generation of reactive oxygen species, activation status, inflammatory cytokine profile, and type I IFN expression and signatures. The capacity of LDGs to kill endothelial cells and their antiangiogenic potential were also assessed. LDGs display an activated phenotype, secrete increased levels of type I IFNs, TNF-alpha, and IFN-gamma, but show impaired phagocytic potential. LDGs induce significant endothelial cell cytotoxicity and synthesize sufficient levels of type I IFNs to disrupt the capacity of endothelial progenitor cells to differentiate into mature endothelial cells. LDG depletion restores the functional capacity of endothelial progenitor cells. We conclude that lupus LDGs are proinflammatory and display pathogenic features, including the capacity to synthesize type I IFNs. They may play an important dual role in premature cardiovascular disease development in systemic lupus erythematosus by simultaneously mediating enhanced vascular damage and inhibiting vascular repair.

Indexed as

AdultCells, CulturedCell SeparationEndothelium, VascularFemaleGranulocytesHumansInflammation MediatorsInterferon-alphaInterferon Type ILeukocyte CountLupus Erythematosus, SystemicMaleMyeloid Progenitor CellsNeutrophilsInflammation MediatorsInterferon-alphaInterferon Type I

Identifiers

PMID20164424
PMCPMC2929645
OpenAlexW1564279536

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.