Evidence map›Paper›PMID 26907212›Full record

ReviewAnnual review of immunology2016

Autoantigens as Partners in Initiation and Propagation of Autoimmune Rheumatic Diseases.

Antony Rosen, Livia Casciola-Rosen

Open access · greenAbstract readReview
In one paragraph

Review in Annual review of immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
5.4field-weighted citation impact, top 5% 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

38 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Autoimmunity: the neoantigen hypothesis.Frontiers in immunology · 2024
    Article
  11. Review
  12. Pathogenesis of autoimmune disease.Nature reviews. Nephrology · 2023
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. IMMUNOEDITING IN AUTOIMMUNE RHEUMATIC DISEASES.Transactions of the American Clinical and Climatological Association · 2022
    Article
  18. Article
  19. Review
  20. 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

2 authors at 1 institution in 1 country.

Antony RosenDivision of Rheumatology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21224; email: arosen@jhmi.edu , lcr@jhmi.edu.
Livia Casciola-RosenDivision of Rheumatology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21224; email: arosen@jhmi.edu , lcr@jhmi.edu.
Johns Hopkins Medicine · US

Funding

Apoptosis in Sjogrens SyndromeR37DE012354 · NIDCR · JOHNS HOPKINS UNIVERSITY · PI ROSEN, ANTONY · 2002 to 2011
$5.3M
Mechanisms in Sjogrens SyndromeR01DE012354 · NIDCR · JOHNS HOPKINS UNIVERSITY · PI ROSEN, ANTONY · 1998 to 2017
$3.4M
NIDCR NIH HHS R01 DE012354NIDCR NIH HHS R37 DE012354
6 · The paper itself

Abstract

Systemic autoimmune diseases are characterized by specific targeting of a limited group of ubiquitously expressed autoantigens by the immune system. This review examines the mechanisms underlying their selection as immune targets. Initiation of autoimmune responses likely reflects the presentation of antigens with a distinct structure not previously encountered by the immune system, in a proimmune context (injury, malignancy, or infection). Causes of modified structure include somatic mutation and posttranslational modifications (including citrullination and proteolysis). Many autoantigens are components of multimolecular complexes, and some of the other components may provide adjuvant activity. Propagation of autoimmune responses appears to reflect a bidirectional interaction between the immune response and the target tissues in a mutually reinforcing cycle: Immune effector pathways generate additional autoantigen, which feeds further immune response. We propose that this resonance may be a critical principle underlying disease propagation, with specific autoantigens functioning as the hubs around which amplification occurs.

Indexed as

Adjuvants, ImmunologicAnimalsAutoantigensAutoimmune DiseasesAutoimmunityFeedback, PhysiologicalHumansImmune ToleranceImmunodominant EpitopesMultiprotein ComplexesRheumatic DiseasesStructure-Activity RelationshipAdjuvants, ImmunologicAutoantigensImmunodominant EpitopesMultiprotein Complexesautoantibodiesimmunodominancemodified structure

Identifiers

PMID26907212
PMCPMC6547816
OpenAlexW2287248643

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.