Evidence map›Paper›PMID 26683148›Full record

ReviewImmunological reviews2016

SLE-associated risk factors affect DC function.

Myoungsun Son, Sun Jung Kim, Betty Diamond

Abstract readReview
In one paragraph

Review in Immunological reviews, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
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

16 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Investigations intoLupus science & medicine · 2021
    Article
  6. Review
  7. HMGB1 in Systemic Lupus Erythematosus.Frontiers in immunology · 2020
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Effects of 1,25(OH)Journal of cellular and molecular medicine · 2017
    Article
  13. Review
  14. Article
  15. Article
  16. Metabolic Factors that Contribute to Lupus Pathogenesis.Critical reviews in immunology · 2016
    Review
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.

Myoungsun SonThe Feinstein Institute for Medical Research, Center for Autoimmune and Musculoskeletal Diseases, Manhasset, NY, USA.
Sun Jung KimThe Feinstein Institute for Medical Research, Center for Autoimmune and Musculoskeletal Diseases, Manhasset, NY, USA.
Betty DiamondThe Feinstein Institute for Medical Research, Center for Autoimmune and Musculoskeletal Diseases, Manhasset, NY, USA.

Funding

Toward a new approach to SLE therapyR01AR057084 · NIAMS · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI DIAMOND, BETTY · 2010 to 2014
$1.8M
The Blimp-1 SLE risk variant regulates inflammatory function in dendritic cellsR01AR065209 · NIAMS · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI KIM, SUN JUNG · 2014 to 2017
$1.8M
Regulation of LAIR-1 in LupusK01AR065506 · NIAMS · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI SON, MYOUNGSUN · 2014 to 2018
$639k
Function of Blimp1/prdm-1 in dendritic cells in the generation of autoantibodiesK01AR059378 · NIAMS · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI KIM, SUN JUNG · 2010 to 2014
$568k
NIAMS NIH HHS K01 AR059378NIAMS NIH HHS K01 AR065506NIAMS NIH HHS K01 AR59378NIAMS NIH HHS R01 AR057084NIAMS NIH HHS R01 AR065209
6 · The paper itself

Abstract

Numerous risk alleles for systemic lupus erythematosus (SLE) have now been identified. Analysis of the expression of genes with risk alleles in cells of hematopoietic origin demonstrates them to be most abundantly expressed in B cells and dendritic cells (DCs), suggesting that these cell types may be the drivers of the inflammatory changes seen in SLE. DCs are of particular interest as they act to connect the innate and the adaptive immune response. Thus, DCs can transform inflammation into autoimmunity, and autoantibodies are the hallmark of SLE. In this review, we focus on mechanisms of tolerance that maintain DCs in a non-activated, non-immunogenic state. We demonstrate, using examples from our own studies, how alterations in DC function stemming from either DC-intrinsic abnormalities or DC-extrinsic regulators of function can predispose to autoimmunity.

Indexed as

Adaptive ImmunityAllelesAutoantibodiesB-LymphocytesDendritic CellsGene-Environment InteractionGenetic Predisposition to DiseaseImmune ToleranceImmunity, InnateLupus Erythematosus, SystemicPolymorphism, GeneticRisk FactorsAutoantibodiesdendritic cellsimmune tolerancerisk allelessystemic lupus

Identifiers

PMID26683148
PMCPMC4685736

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.