Evidence map›Paper›PMID 21158976›Full record

ReviewJournal of internal medicine2011

Moving towards a cure: blocking pathogenic antibodies in systemic lupus erythematosus.

B Diamond, O Bloom, Y Al Abed, C Kowal, P T Huerta, B T Volpe

Registry-linked trialAbstract readReview
In one paragraph

Review in Journal of internal medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06255743 (), which is not on this map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.7field-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.

NCT06255743 naunknown statusnot on this mapstarted 2024, after this paper: background citation

(Anti-Ribosomal P Protein,Anti-U1 RNP, Anti-Nucleosome and Anti-Double Strad DNA Antibodies) Correlate With Depression and Anxiety in Systemic Lupus Erythematosus Patients

TypeinterventionalSponsorSohag UniversityRan2024 to 2025Enrolled50ConditionsSystemic Lupus ErythematosusArmsAnti-Ribosomal P Protein,Anti-U1 RNP, Anti-Nucleosome and Anti-Double Strad DNA Antibodies
3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 49 citations in OpenAlex.

  1. Trial
  2. Review
  3. Peptide-based immunotherapy in lupus: Where are we now?Rheumatology and immunology research · 2023
    Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Brain-reactive antibodies and disease.Annual review of immunology · 2013
    Review
  18. Article
  19. A model for lupus brain disease.Immunological reviews · 2012
    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

6 authors at 2 institutions in 1 country.

B DiamondAutoimmune & Musculoskeletal Disease Center, The Feinstein Institute for Medical Research, Manhasset, NY 11030, USA. bdiamond@nshs.edu
O Bloom
Y Al Abed
C Kowal
P T Huerta
B T Volpe
Feinstein Institute for Medical Research · USCornell University · US

Funding

The Monoclonal Antibody and Reagent CoreP01AI073693 · NIAID · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI Cynthia Aranow · 2008 to 2026
$45.8M
Antibodies to NR2 in SLER01AR049126 · NIAMS · YESHIVA UNIVERSITY · PI DIAMOND, BETTY · 2002 to 2011
$3.8M
Toward a new approach to SLE therapyR01AR057084 · NIAMS · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI DIAMOND, BETTY · 2010 to 2014
$1.8M
Anti-Microbial Antibodies Induce Neuropsychiatric SyndromesR01MH081801 · NIMH · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI DIAMOND, BETTY · 2007 to 2011
$1.8M
NIAID NIH HHS P01 AI073693NIAMS NIH HHS R01 AR049126NIAMS NIH HHS R01 AR057084NIMH NIH HHS R01 MH081801
6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) is characterized by the presence of autoantibodies that can mediate tissue damage in multiple organs. The underlying aetiology of SLE autoantibodies remains unknown, and treatments aimed at eliminating B cells, or limiting their function, have demonstrated limited therapeutic benefit. Thus, the current therapies for SLE are based on the concept of nonspecific immunosuppression and consist of nonsteroidal anti-inflammatory drugs (NSAIDS), corticosteroids, anti-malarials and cytotoxic drugs, all of which have serious adverse side effects including organ damage. The major auto-specificity in SLE is double-stranded (ds) DNA. Many anti-dsDNA antibodies cross-react with non-DNA antigens that may be the direct targets for their pathogenic activity. Studying anti-dsDNA antibodies present in SLE patients and in animal models of lupus, we have identified a subset of anti-dsDNA antibodies which is pathogenic in the brain as well as in the kidney. We have recently demonstrated that specific peptides, or small molecules, can protect target organs from antibody-mediated damage. Thus, it might be possible to treat the aspects of autoimmune disease without inducing major immunosuppression and ensuing infectious complications.

Indexed as

AnimalsAntibodies, AntinuclearAutoantibodiesAutoimmune DiseasesDisease Models, AnimalDNAHumansLupus Erythematosus, SystemicLupus Vasculitis, Central Nervous SystemMiceReceptors, N-Methyl-D-AspartateAntibodies, AntinuclearAutoantibodiesDNAReceptors, N-Methyl-D-Aspartate

Identifiers

PMID21158976
PMCPMC3069637
OpenAlexW1549213298

What OpenQuestion holds

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Registered trials

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.