From Infection to Autoimmunity
Abstract
We have investigated two models of virally-induced autoimmune myocarditis in mice using widely different infectious agents. Infection of susceptible BALB/c mice with either Coxsackievirus or murine cytomegalovirus results in the development of acute myocarditis from day 7-14 after infection, and chronic myocarditis from day 28 onwards. The chronic phase of myocarditis is associated with mononuclear infiltration of the myocardium and the production of autoantibodies to cardiac myosin, although infectious virus cannot be detected past day 14 of infection. T cells and autoantibodies have been shown to be important for the development of autoimmune myocarditis. Many researchers have investigated the role of molecular mimicry in the development of myocarditis after viral infection. This review explores the 'adjuvant' effect of infection on the innate immune response and how this determines the progression to autoimmune disease. We show that NK cells protect against the development of disease, while complement and complement receptors are involved in the development of autoimmune myocarditis induced by inoculation with virus or cardiac myosin, respectively. Our results suggest that the innate immune response to viral and self-antigens may determine whether susceptible strains of mice progress to chronic autoimmune disease. These findings have broad implications for understanding the role of infection in inducing autoimmune disease.
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Both the mRNA against the SARS-CoV-2 spike protein and the lipid nanoparticle vehicle could provide the adjuvant effect needed to promote myocarditis following vaccination with an mRNA vaccine.
“Possibly both the mRNA against the SARS-CoV-2 spike protein and the lipid nanoparticle vehicle could provide the adjuvant effect needed to promote myocarditis following vaccination with an mRNA vaccine. 35,51,198”
From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [35]
This time course is the same as observed with the autoimmune CVB3 and murine cytomegalovirus models of myocarditis and EAM.
“This time course is the same as is observed with the autoimmune CVB3 and murine cytomegalovirus models of myocarditis and EAM (Table S1). 35,124,170,188”
From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [35]
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Women and Autoimmune Diseases1
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Natural Killer Cells Limit Cardiac Inflammation and Fibrosis by Halting Eosinophil Infiltration
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Animal Models for Autoimmune Myocarditis and Autoimmune Thyroiditis
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Self-citationFindings and conclusions from CMV hyperimmune globulin treatment trials
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Fatal Eosinophilic Myocarditis Develops in the Absence of IFN-γ and IL-17A
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- Authors
- Fairweather, D., Kaya, Z., Shellam, G. R., Lawson, C. M., & Rose, N. R.
- Affiliations
- Johns Hopkins University (US)
- The University of Western Australia (AU)
- Murdoch University (AU)
- Venue
- Journal of Autoimmunity
- Publisher
- Elsevier BV
- Published
- 2001-05
- Volume
- 16
- Issue
- 3
- Pages
- 175-186
- ISSN
- 0896-8411 (ISSN-L)
- OpenAlex
- W2076160664
- Cited by
- 328
- References
- 109
- Citations by year
- 2026: 8 · 2025: 7 · 2024: 15 · 2023: 11 · 2022: 10 · 2021: 6 · 2020: 6 · 2019: 4 · 2018: 2 · 2017: 3 · 2016: 14 · 2015: 14 · 2014: 10 · 2013: 12 · 2012: 15
- FWCI
- 14.45
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Autoimmunity (publishedVersion)
- PubMed (publishedVersion)
- Murdoch University Research Portal (submittedVersion)
- Funders
- Deutsche Herzstiftung
- National Institutes of Health
- National Health and Medical Research Council
- National Medical Research Council
- National Heart, Lung, and Blood Institute (HL-33878, R01HL033878)
- National Institute of Environmental Health Sciences (ES99003)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Viral Infections and Immunology Research
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Health Sciences › Medicine › Ophthalmology › Ocular Diseases and Behçet’s Syndrome
- Keywords
- Coxsackie virus, murine cytomegalovirus, molecular mimicry, innate immune response, natural killer cells, complement system, complement receptors, mononuclear cell infiltration, T cells, autoimmunity, BALB/c mice
- MeSH terms
- Animals, Autoimmune Diseases, Complement System Proteins, Coxsackievirus Infections, Herpesviridae Infections, Humans, Immunity, Active, Immunity, Innate, Killer Cells, Natural, Myocarditis, Autoimmunity, Cytokines, Muromegalovirus, Mice
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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