Evidence map›Paper›PMID 9761770›Full record

ReviewFASEB journal : official publication of the Federation of American Societies for Experimental Biology1998

Molecular mimicry and immune-mediated diseases.

M B Oldstone

Open access · bronzeAbstract readReview
In one paragraph

Review in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 186 papers.

0numbers the graph read from it
0cells of the map it votes in
186citing papers in PubMed
19.1field-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

186 citing papers in PubMed, 604 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Understanding Autoimmune Response Mechanisms in Leprosy.Indian dermatology online journal · 2025
    Article
  6. Article
  7. Article
  8. Article
  9. Immune Camouflage inClinical ophthalmology (Auckland, N.Z.) · 2025
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article

126 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

1 author at 1 institution in 2 countries.

M B OldstoneViral Immunobiology Laboratory, Division of Virology, The Scripps Research Institute,Department of Neuropharmacology, La Jolla, California 92037, USA. mbaobo@scripps.edu
Scripps Research Institute · US

Funding

VIROLOGY AND IMMUNOLOGY OF AGINGP01AG004342 · NIA · SCRIPPS RESEARCH INSTITUTE, THE · PI OLDSTONE, MICHAEL B · 1985 to 2008
$12.9M
PATHOGENESIS OF PERSISTENT VIRAL INFECTIONR01AI009484 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI OLDSTONE, MICHAEL B · 1985 to 2016
$7.2M
PATHOGENESIS OF PERSISTENT VIRAL INFECTIONR37AI009484 · NIAID · SCRIPPS RESEARCH INSTITUTE · PI OLDSTONE, MICHAEL B · 1988 to 1997
–
NIAID NIH HHS AI09484NIAID NIH HHS R01 AI009484NIA NIH HHS AG04342NIA NIH HHS P01 AG004342
6 · The paper itself

Abstract

Molecular mimicry has been proposed as a pathogenetic mechanism for autoimmune disease, as well as a probe useful in uncovering its etiologic agents. The hypothesis is based in part on the abundant epidemiological, clinical, and experimental evidence of an association of infectious agents with autoimmune disease and observed cross-reactivity of immune reagents with host 'self' antigens and microbial determinants. For our purpose, molecular mimicry is defined as similar structures shared by molecules from dissimilar genes or by their protein products. Either the molecules' linear amino acid sequences or their conformational fits may be shared, even though their origins are as separate as, for example, a virus and a normal host self determinant. An immune response against the determinant shared by the host and virus can evoke a tissue-specific immune response that is presumably capable of eliciting cell and tissue destruction. The probable mechanism is generation of cytotoxic cross-reactive effector lymphocytes or antibodies that recognize specific determinants on target cells. The induction of cross-reactivity does not require a replicating agent, and immune-mediated injury can occur after the immunogen has been removed a hit-and-run event. Hence, the viral or microbial infection that initiates the autoimmune phenomenon may not be present by the time overt disease develops. By a complementary mechanism, the microbe can induce cellular injury and release self antigens, which generate immune responses that cross-react with additional but genetically distinct self antigens. In both scenarios, analysis of the T cells or antibodies specifically engaged in the autoimmune response and disease provides a fingerprint for uncovering the initiating infectious agent.

Indexed as

Molecular MimicryAnimalsAntigensAutoantibodiesAutoimmune DiseasesCross ReactionsDiabetes Mellitus, Type 1Genetic Predisposition to DiseaseHLA AntigensHLA-B27 AntigenHumansMiceMice, TransgenicMolecular StructureRabbitsT-Lymphocytes, CytotoxicAntigensAutoantibodiesHLA AntigensHLA-B27 Antigen

Identifiers

PMID9761770
PMCPMC7164021
OpenAlexW2142575954

What OpenQuestion holds

Textmetadata
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.