Evidence map›Paper›PMID 28620081›Full record

ReviewJournal of the American Society of Nephrology : JASN2017

Re-Examining Neutrophil Participation in GN.

Dawn J Caster, David W Powell, Irina Miralda, Richard A Ward, Kenneth R McLeish

Erratum issuedOpen access · bronzeAbstract readReview
In one paragraph

Review in Journal of the American Society of Nephrology : JASN, 2017. 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 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

8 citing papers in PubMed, 18 citations in OpenAlex.

  1. Kidney Disease as a Driver of Immunosenescence: Mechanisms and Potential Interventions.Journal of the American Society of Nephrology : JASN · 2026
    Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Therapeutic targeting of neutrophil exocytosis.Journal of leukocyte biology · 2020
    Review
  7. Article
  8. IL-17C/IL-17 Receptor E Signaling in CD4Journal of the American Society of Nephrology : JASN · 2018
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Dawn J CasterDivision of Nephrology and Hypertension, Department of Medicine, University of Louisville School of Medicine, Louisville, Kentucky, dawn.caster@louisville.edu.
David W PowellDivision of Nephrology and Hypertension, Department of Medicine, University of Louisville School of Medicine, Louisville, Kentucky.
Irina MiraldaDepartment of Microbiology and Immunology, University of Louisville School of Medicine, Louisville, Kentucky.
Richard A WardDivision of Nephrology and Hypertension, Department of Medicine, University of Louisville School of Medicine, Louisville, Kentucky.
Kenneth R McLeishDivision of Nephrology and Hypertension, Department of Medicine, University of Louisville School of Medicine, Louisville, Kentucky.
University of Louisville · US

Funding

Nephritogenic autoantibodies in systemic lupusK08DK102542 · NIDDK · UNIVERSITY OF LOUISVILLE · PI CASTER, DAWN · 2016 to 2020
$817k
Identification of diagnostic markers for lupus nephritisR21AI103980 · NIAID · UNIVERSITY OF LOUISVILLE · PI MCLEISH, KENNETH R, POWELL, DAVID W. · 2013 to 2014
$422k
Mechanism of Neutrophil ActivationI01BX001838 · VA · LOUISVILLE VA MEDICAL MEDICAL CENTER · PI MCLEISH, KENNETH R · 2013 to 2016
–
BLRD VA I01 BX001838NIAID NIH HHS R21 AI103980NIDDK NIH HHS K08 DK102542
6 · The paper itself

Abstract

Significant advances in understanding the pathogenesis of GN have occurred in recent decades. Among those advances is the finding that both innate and adaptive immune cells contribute to the development of GN. Neutrophils were recognized as key contributors in early animal models of GN, at a time when the prevailing view considered neutrophils to function as nonspecific effector cells that die quickly after performing antimicrobial functions. However, advances over the past two decades have shown that neutrophil functions are more complex and sophisticated. Specifically, research has revealed that neutrophil survival is regulated by the inflammatory milieu and that neutrophils demonstrate plasticity, mediate microbial killing through previously unrecognized mechanisms, demonstrate transcriptional activity leading to the release of cytokines and chemokines, interact with and regulate cells of the innate and adaptive immune systems, and contribute to the resolution of inflammation. Therefore, neutrophil participation in glomerular diseases deserves re-evaluation. In this review, we describe advances in understanding classic neutrophil functions, review the expanded roles of neutrophils in innate and adaptive immune responses, and summarize current knowledge of neutrophil contributions to GN.

Indexed as

Adaptive ImmunityAnimalsGlomerulonephritisHumansImmunity, InnateNeutrophil InfiltrationNeutrophilsglomerular diseaseglomerulonephritisimmunologyneutrophil

Identifiers

PMID28620081
PMCPMC5533240
OpenAlexW2624936434

What OpenQuestion 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 OpenQuestion graph.