Evidence map›Paper›PMID 36653319›Full record

ArticleClinical and translational medicine2023

CD98 defines a metabolically flexible, proinflammatory subset of low-density neutrophils in systemic lupus erythematosus.

Katherine R Martin, Jessica A Day, Jacinta A Hansen, Damian B D'Silva, Huon L Wong, Alexandra Garnham, Jarrod J Sandow, Brunda Nijagal, Nicholas Wilson, Ian P Wicks

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Clinical and translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

6 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Immunometabolism in systemic lupus erythematosus.Nature reviews. Rheumatology · 2025
    Review
  5. Review
  6. Article
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

10 authors at 4 institutions in 1 country.

Katherine R MartinWalter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia.ORCID 0000-0001-9453-9573
Jessica A DayWalter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia.
Jacinta A HansenWalter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia.
Damian B D'SilvaWalter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia.
Huon L WongWalter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia.
Alexandra GarnhamWalter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia.
Jarrod J SandowWalter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia.
Brunda NijagalMetabolomics Australia, Bio21 Institute of Molecular Science and Biotechnology, University of Melbourne, Parkville, Victoria, Australia.
Nicholas WilsonCSL, Parkville, Victoria, Australia.
Ian P WicksWalter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia.
The University of Melbourne · AUWalter and Eliza Hall Institute of Medical Research · AUThe Royal Melbourne Hospital · AUParks Victoria · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLow-density neutrophils (LDN) are a distinct subset of neutrophils rarely detected in healthy people but appear in the blood of patients with autoimmune diseases, including systemic lupus erythematosus (SLE), and are mobilised in response to granulocyte colony-stimulating factor (G-CSF). The aim of this study was to identify novel mechanisms responsible for the pathogenic capacity of LDN in SLE.

methodsNeutrophils were isolated from donors treated with G-CSF, and whole-cell proteomic analysis was performed on LDN and normal-density neutrophils.

resultsCD98 is significantly upregulated in LDN from G-CSF donors and defines a subset of LDN within the blood of SLE patients. CD98 is a transmembrane protein that dimerises with L-type amino acid transporters. We show that CD98 is responsible for the increased bioenergetic capacity of LDN. CD98 on LDN mediates the uptake of essential amino acids that are used by mitochondria to produce adenosine triphosphate, especially in the absence of glucose. Inhibition of CD98 reduces the metabolic flexibility of this population, which may limit their pathogenic capacity. CD98

conclusionsCD98 provides a phenotypic marker for LDN that facilitates identification of this population without density-gradient separation and represents a novel therapeutic target to limit its pathogenic capacity.

Indexed as

Fusion Regulatory Protein-1Lupus Erythematosus, SystemicNeutrophilsCytokinesGranulocyte Colony-Stimulating FactorHumansProteomicsCytokinesFusion Regulatory Protein-1Granulocyte Colony-Stimulating FactorCD98granulocyte colony-stimulating factorlow-density neutrophilssystemic lupus erythematosus

Identifiers

PMID36653319
PMCPMC9849148
OpenAlexW4317373328

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.