Th2 Regulation of Viral Myocarditis in Mice: Different Roles for TLR3 versus TRIF in Progression to Chronic Disease
Open accessAbstract
Viral infections are able to induce autoimmune inflammation in the heart. Here, we investigated the role of virus-activated Toll-like receptor (TLR)3 and its adaptor TRIF on the development of autoimmune coxsackievirus B3 (CVB3) myocarditis in mice. Although TLR3- or TRIF-deficient mice developed similarly worse acute CVB3 myocarditis and viral replication compared to control mice, disease was significantly worse in TRIF compared to TLR3-deficient mice. Interestingly, TLR3-deficient mice developed an interleukin (IL)-4-dominant T helper (Th)2 response during acute CVB3 myocarditis with elevated markers of alternative activation, while TRIF-deficient mice elevated the Th2-associated cytokine IL-33. Treatment of TLR3-deficient mice with recombinant IL-33 improved heart function indicating that elevated IL-33 in the context of a classic Th2-driven response protects against autoimmune heart disease. We show for the first time that TLR3 versus TRIF deficiency results in different Th2 responses that uniquely influence the progression to chronic myocarditis.
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Following infection, viruses and heart antigens resulting from cardiac damage trigger innate immune responses by engaging TLRs, potentially leading to activation of antiviral adaptive immunity and B cells and T cells targeting cardiac autoantigens.
“Following infection, viruses and heart antigens resulting from cardiac damage trigger innate immune responses by engaging TLRs, potentially leading to the activation of antiviral adaptive immunity and B cells and T cells targeting cardiac autoantigens”
From Autoimmune Myocarditis, Old Dogs and New Tricks. (2024) · cites this paper as [148]
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Experimental — accuracy not yet measuredElevated circulating cytokines could increase myocarditis, as shown when recombinant TNFα, IL-1β, or IL-33 was administered in coxsackievirus B3 virus-only or autoimmune CVB3 animal models.
“In this context, elevated circulating cytokines could increase myocarditis as has been shown previously when recombinant TNF α (tumor necrosis factor-alpha), IL (interleukin)-1 β , or IL-33 was administered in coxsackievirus B3 (CVB3) virus-only or autoimmune CVB3 animal models.”
From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [42]
Results §3.7 reports that recombinant IL-33 increased acute CVB3 myocarditis in wild-type mice, and Methods §2.1 identifies the model as involving infectious virus and heart tissue. The paper does not report administering recombinant TNFα or IL-1β, measuring elevated circulating cytokines, or testing a virus-only model. Results §3.8 also finds that IL-33 improved cardiac function in TLR3-deficient mice, so its effects depend on the setting. (LLM, conf=0.88)
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Self-citation
- Authors
- Abston, E. D., Coronado, M. J., Bucek, A., Bedja, D., Shin, J., Kim, J. B., Kim, E., Gabrielson, K. L., Georgakopoulos, D., Mitzner, W., & Fairweather, D.
- Affiliations
- Johns Hopkins University (US)
- CVRx (United States) (US)
- Corresponding author
- Fairweather, DeLisa
- ORCID
- Venue
- Clinical and Developmental Immunology
- Publisher
- Wiley
- Published
- 2012
- Volume
- 2012
- Pages
- 1-12
- ISSN
- 1740-2522 (ISSN-L)
- 1740-2530
- PMC
- PMC3195533
- OpenAlex
- W2055374064
- Cited by
- 94
- References
- 34
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 8 · 2023: 8 · 2022: 5 · 2021: 12 · 2020: 5 · 2019: 4 · 2018: 7 · 2017: 3 · 2016: 5 · 2015: 4 · 2014: 9 · 2013: 9 · 2012: 10
- FWCI
- 6.14
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Clinical and Developmental Immunology (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institutes of Health (HL087033)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Viral Infections and Immunology Research
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Keywords
- viral myocarditis, coxsackievirus B3, Th2 immune response, TLR3, TRIF, Toll-like receptor signaling, IL-33, IL-4, M2 macrophages, autoimmune heart disease, chronic myocarditis, cardiac function
- MeSH terms
- Interleukin-33, Acute Disease, Animals, Chronic Disease, Coxsackievirus Infections, Enterovirus, Gene Expression Regulation, Interleukins, Mice, Inbred C57BL, Myocarditis, Virus Replication, Autoimmunity, Interleukin-4, Mice, Knockout, Th2 Cells, Disease Progression, Adaptor Proteins, Vesicular Transport, Toll-Like Receptor 3, Mice
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