Evidence map›Paper›PMID 22209691›Full record

ReviewCurrent opinion in immunology2012

Autoantigenesis: the evolution of protein modifications in autoimmune disease.

Hester A Doyle, Mark J Mamula

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed
4.0field-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

85 citing papers in PubMed, 144 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. Unmet needs in autoimmune liver diseases.Current opinion in immunology · 2025
    Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Antibody profiles in the mosaic of 'seronegative' APS syndrome.Clinical and experimental immunology · 2024
    Article
  13. Article
  14. Article
  15. Review
  16. The persistent inflammation in COPD: is autoimmunity the core mechanism?European respiratory review : an official journal of the European Respiratory Society · 2024
    Review
  17. Review
  18. Review
  19. Article
  20. Article

25 more citing papers are in PubMed but not listed here.

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.

Hester A DoyleSection of Rheumatology, Yale University School of Medicine, New Haven, CT, United States.
Mark J Mamula
Yale University · US

Funding

TOLERANCE AND AUTOIMMUNITY IN RF TRANSGENIC MICEP01AI036529 · NIAID · YALE UNIVERSITY · PI FLAVELL, RICHARD A · 1994 to 2006
$9.4M
Post Translational Modifications in Tolerance and AutoimmunityR01AI048120 · NIAID · YALE UNIVERSITY · PI MAMULA, MARK J · 2001 to 2019
$5.6M
MOLECULAR MECHANISMS OF LYMPHOCYTE INTERACTIONS IN SLER01AR041032 · NIAMS · YALE UNIVERSITY · PI MAMULA, MARK J · 1997 to 2011
$2.4M
EGFR Peptides as Vaccines in Anti-Tumor ImmunityR42CA128165 · NCI · L2 DIAGNOSTICS, LLC · PI MAMULA, MARK J · 2010 to 2013
$1.4M
Modified HER-2 Tumor Antigens for Vaccination in CancerR42CA106107 · NCI · L2 DIAGNOSTICS, LLC · PI MAMULA, MARK J. · 2006 to 2007
$1.1M
POST TRANSLATIONAL MODIFICATIONS AND AUTOIMMUNITYR21AI048120 · NIAID · YALE UNIVERSITY · PI MAMULA, MARK J. · 2000 to 2000
$323k
The contribution of protein methylation to the development of sytemic lupus erythR03AR057155 · NIAMS · YALE UNIVERSITY · PI DOYLE, HESTER A · 2009 to 2011
$244k
Isoaspartyl Modified Tumor Antigens for VaccinationR41CA101542 · NCI · L2 DIAGNOSTICS, LLC · PI MAMULA, MARK J. · 2004 to 2004
$100k
NCI NIH HHS R41 CA101542NCI NIH HHS R42 CA106107NCI NIH HHS R42 CA128165NIAID NIH HHS P01 AI036529NIAID NIH HHS R01 AI048120NIAID NIH HHS R21 AI048120NIAMS NIH HHS R01 AR041032NIAMS NIH HHS R03 AR057155
6 · The paper itself

Abstract

Protein targets in autoimmune disease vary in location, originating within cells as in system lupus erythematosus (SLE), or found on cell surfaces or in extracellular spaces. The term 'autoantigenesis' is first defined here as the changes that arise in self-proteins as they break self-tolerance and trigger autoimmune B and/or T cell responses. As illustrated in many studies, between 50 and 90% of the proteins in the human body acquire post-translational modification. In some cases, it may be that these modifications are necessary for the biological functions of proteins of the cells in which they reside or as extracellular mediators. Summarized herein, it is clear that some post-translational modifications can create new self-antigens by altering immunologic processing and presentation. While many protein modifications exist, we will focus on those created, amplified, or altered in the context of inflammation or other immune system responses. Finally, we will address how post-translational modifications in self-antigens may affect the analyses of B and T cell specificity, current diagnostic techniques, and/or the development of immunotherapies for autoimmune diseases.

Indexed as

Protein Processing, Post-TranslationalAnimalsAntigen PresentationAutoantigensAutoimmune DiseasesB-LymphocytesHumansT-LymphocytesAutoantigens

Identifiers

PMID22209691
PMCPMC3288476
OpenAlexW2056670275

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.