Evidence map›Paper›PMID 27780774›Full record

ReviewClinical immunology (Orlando, Fla.)2017

The contribution of the programmed cell death machinery in innate immune cells to lupus nephritis.

FuNien Tsai, Harris Perlman, Carla M Cuda

Open access · greenAbstract readReview
In one paragraph

Review in Clinical immunology (Orlando, Fla.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

10 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Comprehensive analysis of myeloid reporter mice.bioRxiv : the preprint server for biology · 2025
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. 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

3 authors at 1 institution in 1 country.

FuNien TsaiNorthwestern University, Feinberg School of Medicine, Department of Medicine, Division of Rheumatology, 240 East Huron Street, Room M300, Chicago, IL 60611, USA. Electronic address: fntsai@u.northwestern.edu.
Harris PerlmanNorthwestern University, Feinberg School of Medicine, Department of Medicine, Division of Rheumatology, 240 East Huron Street, Room M300, Chicago, IL 60611, USA. Electronic address: h-perlman@northwestern.edu.
Carla M CudaNorthwestern University, Feinberg School of Medicine, Department of Medicine, Division of Rheumatology, 240 East Huron Street, Room M300, Chicago, IL 60611, USA. Electronic address: c-cuda@northwestern.edu.
Northwestern University · US

Funding

Small Animal Surgery and HistologyP01HL108795 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LOSORDO, DOUGLAS W · 2011 to 2015
$10.7M
Therapeutic Role for P21 in Suppressing IL-1 Beta Mediated PathologiesR01AR050250 · NIAMS · SAINT LOUIS UNIVERSITY · PI PERLMAN, HARRIS R · 2003 to 2014
$3.0M
Role of BH3-Domain Proteins in the Effector Phase of RAR01AR054796 · NIAMS · SAINT LOUIS UNIVERSITY · PI PERLMAN, HARRIS R · 2008 to 2012
$1.8M
Development of a Novel RA/Atherosclerosis Mouse ModelR01AR064546 · NIAMS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI PERLMAN, HARRIS R · 2013 to 2017
$1.6M
Caspase 8: A Novel Suppressor of Dendritic Cell-Mediated AutoimmunityK01AR064313 · NIAMS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI CUDA, CARLA M · 2013 to 2017
$597k
A novel and improved mouse system for studying macrophage specific gene deletionR21AI092490 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI PERLMAN, HARRIS R, STEHLIK, CHRISTIAN · 2011 to 2012
$419k
NHLBI NIH HHS P01 HL108795NIAID NIH HHS R21 AI092490NIAMS NIH HHS K01 AR064313NIAMS NIH HHS R01 AR050250NIAMS NIH HHS R01 AR054796NIAMS NIH HHS R01 AR064546
6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) is a chronic multi-factorial autoimmune disease initiated by genetic and environmental factors, which in combination trigger disease onset in susceptible individuals. Damage to the kidney as a consequence of lupus nephritis (LN) is one of the most prevalent and severe outcomes, as LN affects up to 60% of SLE patients and accounts for much of SLE-associated morbidity and mortality. As remarkable strides have been made in unlocking new inflammatory mechanisms associated with signaling molecules of programmed cell death pathways, this review explores the available evidence implicating the action of these pathways specifically within dendritic cells and macrophages in the control of kidney disease. Although advancements into the underlying mechanisms responsible for inducing cell death inflammatory pathways have been made, there still exist areas of unmet need. By understanding the molecular mechanisms by which dendritic cells and macrophages contribute to LN pathogenesis, we can improve their viability as potential therapeutic targets to promote remission.

Indexed as

AnimalsApoptosisDendritic CellsHumansImmunity, InnateLupus NephritisMacrophagesDendritic cellLupus nephritisMacrophagesProgrammed cell death

Identifiers

PMID27780774
PMCPMC5401656
OpenAlexW2534967013

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.