Learning from myocarditis: mimicry, chaos and black holes
Open accessAbstract
Autoimmune myocarditis and its sequel, dilated cardiomyopathy, are major causes of heart failure, especially in children and young adults. We have developed animal models to investigate their pathogenesis by infecting genetically susceptible mice with coxsackievirus B3 or by immunizing them with cardiac myosin or its immunodominant peptide. A number of valuable lessons have emerged from our study of this paradigm of an infection-induced autoimmune disease. We understand more clearly how natural autoimmunity, as an important component of normal physiology, must be recalibrated regularly due to changes caused by infection or other internal and external stimuli. A new normal homeostatic platform will be established based on its evolutionary fitness. A loss of homeostasis with out-of-control normal autoimmunity leads to autoimmune disease. It is signified early on by a spread of an adaptive autoimmune response to novel epitopes and neighboring antigens. The progression from infection to normal, well-balanced autoimmunity to autoimmune disease and on to irreversible damage is a complex, step-wise process. Yet, chaos theory provides hope that the pattern is potentially predictable. Infection-induced autoimmune disease represents a sequence of events heading for a train wreck at the end of the line. Our aim in autoimmune disease research must be to stop the train before this happens.
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In lymphocytic myocarditis, autoreactive immune responses, both humoral and cellular, may induce pathogenic inflammation due to tissue damage from repeated viral challenges or molecular mimicry between virus and heart antigens.
“whether due to tissue damage caused by repeated viral challenges or molecular mimicry between virus and heart antigens, autoreactive immune responses, both humoral and cellular, may induce pathogenic inflammation in lymphocytic myocarditis”
From Autoimmune Myocarditis, Old Dogs and New Tricks. (2024) · cites this paper as [145]
“Constructing a model” describes viral injury and molecular mimicry as possible routes to autoimmune myocarditis, and reports that myosin-specific CD4 T cells can induce disease. “Myocarditis and dilated cardiomyopathy” reports heart-reactive autoantibodies but says their role in pathogenesis remains uncertain. The copy does not establish repeated viral challenges or that both humoral and cellular responses induce pathogenic inflammation. (LLM, conf=0.86)
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- Authors
- Rose, N. R.
- Affiliations
- Johns Hopkins University (US)
- Corresponding author
- Rose, Noel R.
- Venue
- F1000Prime Reports
- Publisher
- Faculty Opinions Ltd
- Published
- 2014-05-06
- Volume
- 6
- Pages
- 25-25
- ISSN
- 2051-7599 (ISSN-L)
- PMC
- PMC4018180
- OpenAlex
- W2027575580
- Cited by
- 44
- References
- 44
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 3 · 2023: 2 · 2022: 5 · 2021: 5 · 2020: 7 · 2019: 5 · 2018: 4 · 2017: 2 · 2016: 6 · 2015: 1 · 2014: 2
- FWCI
- 0.59
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- F1000Prime Reports (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Heart, Lung, and Blood Institute (R56HL077611, R01HL077611, R01HL067290, R01HL113008)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Viral Infections and Immunology Research
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- autoimmune myocarditis, dilated cardiomyopathy, heart failure, coxsackievirus B3, cardiac myosin, immunodominant peptides, animal models, chaos theory, mimicry
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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