Evidence map›Paper›PMID 22095454›Full record

ReviewClinical reviews in allergy & immunology2012

Molecular mimicry as a mechanism of autoimmune disease.

Matthew F Cusick, Jane E Libbey, Robert S Fujinami

Open access · bronzeAbstract readReview
In one paragraph

Review in Clinical reviews in allergy & immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 313 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
313citing papers in PubMed, 7 pooled it
5.9field-weighted citation impact, top 3% 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

313 citing papers in PubMed, 7 syntheses or guidelines pooled it, 588 citations in OpenAlex.

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253 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

3 authors at 1 institution in 1 country.

Matthew F CusickDepartment of Pathology, University of Utah, Salt Lake City, UT 84132, USA.
Jane E Libbey
Robert S Fujinami
University of Utah · US

Funding

Virus-Host Interactions that Lead to EpilepsyR01NS065714 · NINDS · UNIVERSITY OF UTAH · PI FUJINAMI, ROBERT S · 2010 to 2018
$2.9M
NINDS NIH HHS R01 NS065714
6 · The paper itself

Abstract

A variety of mechanisms have been suggested as the means by which infections can initiate and/or exacerbate autoimmune diseases. One mechanism is molecular mimicry, where a foreign antigen shares sequence or structural similarities with self-antigens. Molecular mimicry has typically been characterized on an antibody or T cell level. However, structural relatedness between pathogen and self does not account for T cell activation in a number of autoimmune diseases. A proposed mechanism that could have been misinterpreted for molecular mimicry is the expression of dual T cell receptors (TCR) on a single T cell. These T cells have dual reactivity to both foreign and self-antigens leaving the host vulnerable to foreign insults capable of triggering an autoimmune response. In this review, we briefly discuss what is known about molecular mimicry followed by a discussion of the current understanding of dual TCRs. Finally, we discuss three mechanisms, including molecular mimicry, dual TCRs, and chimeric TCRs, by which dual reactivity of the T cell may play a role in autoimmune diseases.

Indexed as

AnimalsAntigensAutoimmune DiseasesAutoimmunityHumansMolecular MimicryReceptors, Antigen, T-CellAntigensReceptors, Antigen, T-Cell

Identifiers

PMID22095454
PMCPMC3266166
OpenAlexW2019355614

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.