Evidence map›Paper›PMID 37390745›Full record

ReviewJournal of autoimmunity2023

Molecular mimicry and autoimmunity in the time of COVID-19.

Manuel Rojas, María Herrán, Carolina Ramírez-Santana, Patrick S C Leung, Juan-Manuel Anaya, William M Ridgway, M Eric Gershwin

Open access · greenAbstract readReview
In one paragraph

Review in Journal of autoimmunity, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 4 pooled it
9.8field-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

36 citing papers in PubMed, 4 syntheses or guidelines pooled it, 64 citations in OpenAlex.

  1. Pooled it
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  4. Pooled it
  5. Review
  6. Review
  7. Article
  8. How to Cure Autoimmune GN and Podocytopathies.Journal of the American Society of Nephrology : JASN · 2026
    Review
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  11. Article
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  19. NETosis: A key player in autoimmunity, COVID-19, and long COVID.Journal of translational autoimmunity · 2025
    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

7 authors at 2 institutions in 2 countries.

Manuel RojasDivision of Rheumatology, Allergy and Clinical Immunology, University of California, Davis, CA, 95616, USA; Center for Autoimmune Diseases Research (CREA), School of Medicine and Health Sciences, Universidad del Rosario, Bogota, Colombia. Electronic address: mrojasquintana@ucdavis.edu.
María HerránCenter for Autoimmune Diseases Research (CREA), School of Medicine and Health Sciences, Universidad del Rosario, Bogota, Colombia.
Carolina Ramírez-SantanaCenter for Autoimmune Diseases Research (CREA), School of Medicine and Health Sciences, Universidad del Rosario, Bogota, Colombia.
Patrick S C LeungDivision of Rheumatology, Allergy and Clinical Immunology, University of California, Davis, CA, 95616, USA.
Juan-Manuel AnayaHealth Research and Innovation Center at Coosalud, Cartagena, 130001, Colombia.
William M RidgwayDivision of Rheumatology, Allergy and Clinical Immunology, University of California, Davis, CA, 95616, USA.
M Eric GershwinDivision of Rheumatology, Allergy and Clinical Immunology, University of California, Davis, CA, 95616, USA.
University of California, Davis · USUniversidad del Rosario · CO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Infectious diseases are commonly implicated as potential initiators of autoimmune diseases (ADs) and represent the most commonly known factor in the development of autoimmunity in susceptible individuals. Epidemiological data and animal studies on multiple ADs suggest that molecular mimicry is one of the likely mechanisms for the loss of peripheral tolerance and the development of clinical disease. Besides molecular mimicry, other mechanisms such as defects in central tolerance, nonspecific bystander activation, epitope-determinant spreading, and/or constant antigenic stimuli, may also contribute for breach of tolerance and to the development of ADs. Linear peptide homology is not the only mechanism by which molecular mimicry is established. Peptide modeling (i.e., 3D structure), molecular docking analyses, and affinity estimation for HLAs are emerging as critical strategies when studying the links of molecular mimicry in the development of autoimmunity. In the current pandemic, several reports have confirmed an influence of SARS-CoV-2 on subsequent autoimmunity. Bioinformatic and experimental evidence support the potential role of molecular mimicry. Peptide dimensional analysis requires more research and will be increasingly important for designing and distributing vaccines and better understanding the role of environmental factors related to autoimmunity.

Indexed as

Autoimmune DiseasesCOVID-19AnimalsAutoimmunityMolecular Docking SimulationMolecular MimicrySARS-CoV-2Autoimmune diseasesAutoimmunityCOVID-19Cross-reactivityMolecular mimicrySARS-CoV-2Vaccines

Identifiers

PMID37390745
PMCPMC10258587
OpenAlexW4380324272

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.