Evidence map›Paper›PMID 36305174›Full record

ReviewImmunological reviews2023

Low-density granulocytes in systemic autoimmunity and autoinflammation.

Carmelo Carmona-Rivera, Mariana J Kaplan

Open access · greenAbstract readReview
In one paragraph

Review in Immunological reviews, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.7field-weighted citation impact, top 5% 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

38 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Review
  3. Dysregulation of U12-Type Splicing in Lupus Neutrophils.Arthritis & rheumatology (Hoboken, N.J.) · 2026
    Article
  4. Article
  5. Integrated single-cell transcriptomic analysis identifiesBiochemistry and biophysics reports · 2026
    Article
  6. Article
  7. Review
  8. Proceedings of the 2Mediterranean journal of rheumatology · 2026
    Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Dysregulation of U12-Type Splicing in Lupus Neutrophils.bioRxiv : the preprint server for biology · 2025
    Article
  18. Article
  19. Review
  20. 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

2 authors at 1 institution in 1 country.

Carmelo Carmona-RiveraSystemic Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland, USA.ORCID 0000-0002-7706-1464
Mariana J KaplanSystemic Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland, USA.ORCID 0000-0003-2968-0815
National Institutes of Health · US

Funding

Systemic AutoimmunityZIAAR041199 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI KAPLAN, MARIANA · 2014 to 2025
$32.5M
Intramural NIH HHS ZIA AR041199
6 · The paper itself

Abstract

A body of evidence has re-energized the interest on the role neutrophils in inflammatory and autoimmune conditions. For decades, neutrophils have been considered a homogenous population. Nevertheless, accumulating evidence suggests that neutrophils are more versatile and heterogeneous than initially considered. The notion of neutrophil heterogeneity has been supported by the identification of low-density granulocytes (LDGs) in systemic lupus erythematosus (SLE) and other systemic autoimmune and autoinflammatory conditions. Transcriptomic, epigenetic, proteomic, and functional analyses support that LDGs are a distinct subset of proinflammatory neutrophils implicated in the pathogenesis of SLE and other autoimmune diseases. Importantly, it remains incompletely characterized whether LDGs detected in other inflammatory/autoimmune conditions display the same phenotype that those present in SLE. A shared feature of LDGs across diseases is their association with vascular damage, an important contributor to morbidity and mortality in chronic inflammatory conditions. Additionally, the lack of specific markers to identify LDGs in circulation or in tissue, makes it a challenge to elucidate their role in the pathogenesis of inflammatory and autoimmune conditions. In this review, we aim to examine the evidence on the biology and the putative pathogenic role of LDGs in systemic autoimmune diseases.

Indexed as

AutoimmunityLupus Erythematosus, SystemicGranulocytesHumansNeutrophilsProteomicsautoimmunityinnate immunityneutrophilssystemic lupus erythematosus

Identifiers

PMID36305174
PMCPMC10050110
OpenAlexW4307499111

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.