Evidence map›Paper›PMID 29497420›Full record

ReviewFrontiers in immunology2018

Infection Elicited Autoimmunity and Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: An Explanatory Model.

Jonas Blomberg, Carl-Gerhard Gottfries, Amal Elfaitouri, Muhammad Rizwan, Anders Rosén

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
10.2field-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

81 citing papers in PubMed, 120 citations in OpenAlex.

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21 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

5 authors at 3 institutions in 2 countries.

Jonas BlombergDepartment of Medical Sciences, Uppsala University, Clinical Microbiology, Academic Hospital, Uppsala, Sweden.
Carl-Gerhard GottfriesGottfries Clinic AB, Mölndal, Sweden.
Amal ElfaitouriDepartment of Infectious Disease and Tropical Medicine, Faculty of Public Health, Benghazi University, Benghazi, Libya.
Muhammad RizwanDepartment of Medical Sciences, Uppsala University, Clinical Microbiology, Academic Hospital, Uppsala, Sweden.
Anders RosénDepartment of Clinical and Experimental Medicine, Division of Cell Biology, Linköping University, Linköping, Sweden.
Uppsala University Hospital · SELinköping University · SEUniversity of Benghazi · LY

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myalgic encephalomyelitis (ME) often also called chronic fatigue syndrome (ME/CFS) is a common, debilitating, disease of unknown origin. Although a subject of controversy and a considerable scientific literature, we think that a solid understanding of ME/CFS pathogenesis is emerging. In this study, we compiled recent findings and placed them in the context of the clinical picture and natural history of the disease. A pattern emerged, giving rise to an explanatory model. ME/CFS often starts after or during an infection. A logical explanation is that the infection initiates an autoreactive process, which affects several functions, including brain and energy metabolism. According to our model for ME/CFS pathogenesis, patients with a genetic predisposition and dysbiosis experience a gradual development of B cell clones prone to autoreactivity. Under normal circumstances these B cell offsprings would have led to tolerance. Subsequent exogenous microbial exposition (triggering) can lead to comorbidities such as fibromyalgia, thyroid disorder, and orthostatic hypotension. A decisive infectious trigger may then lead to immunization against autoantigens involved in aerobic energy production and/or hormone receptors and ion channel proteins, producing postexertional malaise and ME/CFS, affecting both muscle and brain. In principle, cloning and sequencing of immunoglobulin variable domains could reveal the evolution of pathogenic clones. Although evidence consistent with the model accumulated in recent years, there are several missing links in it. Hopefully, the hypothesis generates testable propositions that can augment the understanding of the pathogenesis of ME/CFS.

Indexed as

AutoimmunityModels, BiologicalAutoantigensB-LymphocytesDysbiosisFatigue Syndrome, ChronicGenetic Predisposition to DiseaseHumansImmune ToleranceImmunoglobulin Variable RegionInfectionsPhysical ExertionAutoantigensImmunoglobulin Variable Regionautoimmunitychronic fatigue syndromeirritable bowel syndromemyalgic encephalomyelitispostexertional malaise

Identifiers

PMID29497420
PMCPMC5818468
OpenAlexW2793749585

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.