Evidence map›Paper›PMID 27504587›Full record

ReviewCurrent opinion in immunology2016

DNA-reactive B cells in lupus.

Jolien Suurmond, Justine Calise, Susan Malkiel, Betty Diamond

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 7% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Measurement of circulating CD21Scientific reports · 2022
    Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. DNA as a self-antigen: nature and regulation.Current opinion in immunology · 2018
    Review
  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

4 authors at 2 institutions in 1 country.

Jolien SuurmondCenter for Autoimmune and Musculoskeletal Diseases, The Feinstein Institute for Medical Research, North Shore-LIJ, 350 Community Drive, Manhasset, NY 11030, USA.
Justine CaliseCenter for Autoimmune and Musculoskeletal Diseases, The Feinstein Institute for Medical Research, North Shore-LIJ, 350 Community Drive, Manhasset, NY 11030, USA; PhD Program in Molecular Medicine, Hofstra-Northwell School of Medicine, 500 Hofstra Blvd, Hempstead, NY 11549, USA.
Susan MalkielCenter for Autoimmune and Musculoskeletal Diseases, The Feinstein Institute for Medical Research, North Shore-LIJ, 350 Community Drive, Manhasset, NY 11030, USA.
Betty DiamondCenter for Autoimmune and Musculoskeletal Diseases, The Feinstein Institute for Medical Research, North Shore-LIJ, 350 Community Drive, Manhasset, NY 11030, USA. Electronic address: bdiamond@northwell.edu.
Feinstein Institute for Medical Research · USHofstra University · US

Funding

Toward a new approach to SLE therapyR01AR057084 · NIAMS · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI DIAMOND, BETTY · 2010 to 2014
$1.8M
NIAMS NIH HHS R01 AR057084
6 · The paper itself

Abstract

IgG anti-DNA antibodies are both diagnostic and pathogenic for systemic lupus erythematosus (SLE). They contribute to tissue inflammation through direct tissue binding and to systemic inflammation through activation of Toll-like receptors by nucleic acid-containing immune complexes. IgG DNA-reactive antibodies originate when B cell tolerance mechanisms are impaired. The heterogeneous immune perturbations in SLE lead to the survival and activation of DNA-reactive B cells in various B cell subsets at distinct stages of B cell maturation and differentiation. We propose that the spectrum of B cell alterations and failed tolerance mechanisms for DNA-reactive B cells in lupus patients is best understood by studying genetic risk alleles. This implies that the B cells producing IgG anti-DNA antibodies and the failed tolerance mechanisms(s) will differ across patients. A better understanding of these differences should lead to better patient stratification, improved outcomes of clinical trials, and the identification of novel therapeutic targets.

Indexed as

AllelesAnimalsAntibodies, AntinuclearB-LymphocytesB-Lymphocyte SubsetsDNAGenetic Predisposition to DiseaseGenotypeHumansImmune ToleranceLupus Erythematosus, SystemicRiskAntibodies, AntinuclearDNA

Identifiers

PMID27504587
PMCPMC5125853
OpenAlexW2515254322

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.