Evidence map›Paper›PMID 18756274›Full record

ReviewNature clinical practice. Rheumatology2008

Nature and functions of autoantibodies.

Keith Elkon, Paolo Casali

Open access · greenAbstract readReview
In one paragraph

Review in Nature clinical practice. Rheumatology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 207 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
207citing papers in PubMed, 4 pooled it
11.1field-weighted citation impact, top 1% 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

207 citing papers in PubMed, 4 syntheses or guidelines pooled it, 379 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Guideline
  4. Pooled it
  5. Review
  6. Article
  7. Article
  8. Targeting FcRn for immunomodulation: a promising therapy in autoimmune inflammatory rheumatic diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  9. Article
  10. Pro-Cognitive Effects of IgM Isotype Anti-NMDAR1 Autoantibodies in Mice.bioRxiv : the preprint server for biology · 2026
    Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Identification of Antibodies to Chondrocyte and Synoviocyte Antigens in Equine Osteoarthritis.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2025
    Article
  16. Review
  17. Can we cure vasculitis?Current opinion in immunology · 2025
    Review
  18. Review
  19. Article
  20. Article

147 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 2 institutions in 1 country.

Keith ElkonDivision of Rheumatology, University of Washington School of Medicine, Seattle, WA, USA.
Paolo Casali
University of California, Irvine · USUniversity of Washington · US

Funding

Apoptotic Cells As Immunogens In SLER01AR048796 · NIAMS · UNIVERSITY OF WASHINGTON · PI ELKON, KEITH B. · 2001 to 2010
$2.7M
Nucleoprotein Immune Complexes and Interferon in Diffuse Neuropsychiatric SLER21AR054980 · NIAMS · UNIVERSITY OF WASHINGTON · PI ELKON, KEITH B. · 2007 to 2008
$365k
NIAMS NIH HHS R01 AR048796NIAMS NIH HHS R21 AR054980
6 · The paper itself

Abstract

Antibodies that react with self-molecules occur in healthy individuals and are referred to as natural antibodies or autoantibodies. Natural autoantibodies are mainly IgM, are encoded by unmutated V(D)J genes and display a moderate affinity for self-antigens. They provide a first line of defense against infections, probably serve housekeeping functions and contribute to the homeostasis of the immune system. By contrast, high-affinity, somatically mutated IgG autoantibodies reflect a pathologic process whereby homeostatic pathways related to cell clearance, antigen-receptor signaling or cell effector functions are disturbed. In some autoimmune disorders, autoantibodies might be present before disease onset, show remarkable specificity and serve as biomarkers providing an opportunity for diagnosis and therapeutic intervention. In organ-specific autoimmune diseases, such as myasthenia gravis or pemphigus, autoantibodies directly bind to and injure target organs. In systemic autoimmune diseases, autoantibodies react with free molecules, such as phospholipids, as well as cell surface and nucleoprotein antigens, forming pathogenic antigen-antibody (immune) complexes. These autoantibodies injure tissues and organs through engagement of Fc gammaR activation of complement as well as internalization and activation of Toll-like receptors. Activation of intracellular Toll-like receptors in plasmacytoid dendritic cells leads to the production of type I interferon, whereas engagement of intracellular Toll-like receptors on antigen-presenting cells stimulates cell activation and the production of other inflammatory cytokines. Thus, immune complexes might perpetuate a positive feedback loop amplifying inflammatory responses.

Indexed as

Antibody-Producing CellsAntigen-Antibody ComplexAntigen-Antibody ReactionsAutoantibodiesAutoimmune DiseasesHumansImmunoglobulin GImmunoglobulin MAntigen-Antibody ComplexAutoantibodiesImmunoglobulin GImmunoglobulin M

Identifiers

PMID18756274
PMCPMC2703183
OpenAlexW2167940772

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.