Cardiac myosin-Th17 responses promote heart failure in human myocarditis
Open accessAbstract
In human myocarditis and its sequela dilated cardiomyopathy (DCM), the mechanisms and immune phenotype governing disease and subsequent heart failure are not known. Here, we identified a Th17 cell immunophenotype of human myocarditis/DCM with elevated CD4 + IL17 + T cells and Th17-promoting cytokines IL-6, TGF-β, and IL-23 as well as GM-CSF–secreting CD4 + T cells. The Th17 phenotype was linked with the effects of cardiac myosin on CD14 + monocytes, TLR2, and heart failure. Persistent heart failure was associated with high percentages of IL-17–producing T cells and IL-17–promoting cytokines, and the myocarditis/DCM phenotype included significantly low percentages of FOXP3 + Tregs, which may contribute to disease severity. We demonstrate a potentially novel mechanism in human myocarditis/DCM in which TLR2 peptide ligands from human cardiac myosin stimulated exaggerated Th17-related cytokines including TGF-β, IL-6, and IL-23 from myocarditic CD14 + monocytes in vitro, and an anti-TLR2 antibody abrogated the cytokine response. Our translational study explains how an immune phenotype may be initiated by cardiac myosin TLR ligand stimulation of monocytes to generate Th17-promoting cytokines and development of pathogenic Th17 cells in human myocarditis and heart failure, and provides a rationale for targeting IL-17A as a therapeutic option.
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IL-1β increases serum and cardiac IL-6 levels that are needed to drive Th17 responses, which promote fibrosis and progression to DCM and heart failure in patients with myocarditis and in animal models.
“IL-1 β also increases serum and cardiac IL-6 levels that are needed to drive Th17 responses, which also promote fibrosis and progression to DCM and heart failure in patients with myocarditis and in animal models. 36,165,172-174”
From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [36]
The Results report elevated peripheral-blood IL-6 in patients with myocarditis/DCM and describe IL-6 as necessary for Th17 differentiation. The Discussion links Th17 responses with fibrosis and heart failure in humans, while noting that the human fibrosis finding is correlational and that mouse studies provide additional support. The paper does not show that IL-1β increases serum or cardiac IL-6 levels; it reports IL-1β and IL-6 together as Th17-associated cytokines. (LLM, conf=0.88)
Experimental — accuracy not yet measuredFollowing 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 [64]
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredRecent studies implemented pathogenic T cells as potential diagnostic or therapeutic targets for autoimmune myocarditis including ICI myocarditis, demonstrating promising outcomes at both clinical and preclinical levels.
“Recent studies implemented pathogenic T cells as potential diagnostic or therapeutic targets for autoimmune myocarditis including ICI myocarditis, demonstrating promising outcomes at both clinical and preclinical levels. 51,64,238,254,260,311,312”
From Autoimmune Myocarditis, Old Dogs and New Tricks. (2024) · cites this paper as [64]
The Discussion (page unavailable) identifies Th17 cells as potential therapeutic targets and describes the study as a first step toward improved diagnosis and treatment of human myocarditis. The Introduction also reports reduced myocarditis after anti–IL-23 treatment in a mouse model. The paper does not address ICI myocarditis or demonstrate promising clinical outcomes from implementing T-cell-targeted diagnosis or treatment. (LLM, conf=0.88)
Experimental — accuracy not yet measuredAutoreactive T cells specific for α-MyHC are present in peripheral blood mononuclear cells of patients with myocarditis.
“Subsequent investigations revealed the presence of these autoreactive T cells in the peripheral blood mononuclear cells of patients with myocarditis”
From Autoimmune Myocarditis, Old Dogs and New Tricks. (2024) · cites this paper as [64]
The Results section (“Th17 immunophenotype contributes to myocarditis, DCM, and heart failure”; page unavailable) reports elevated Th17 cells in peripheral blood of patients with myocarditis/DCM. The Methods section (“Phenotyping of blood immune T cells by flow cytometry”; page unavailable) describes measuring these cells in PBMCs, but does not establish that the T cells were specific for α-MyHC. The reported cardiac-myosin responses in PBMCs were attributed to CD14+ monocytes, not antigen-specific T cells. (LLM, conf=0.86)
Experimental — accuracy not yet measuredIn patients with myocarditis, the number of Th17 cells is increased in PBMC and myocardial tissue, and Th17-type cytokine levels are associated with heart failure and nonrecovery conditions.
“in patients with myocarditis, the number of Th17 cells was increased in the PBMC and myocardial tissue, and Th17-type cytokine levels were associated with heart failure and nonrecovery conditions”
From Autoimmune Myocarditis, Old Dogs and New Tricks. (2024) · cites this paper as [64]
The Results report significantly elevated Th17 cells in peripheral blood of myocarditis/DCM patients and associate Th17-related cytokines with heart failure and nonrecovery. Myocardial biopsies showed IL-17A–positive cells in 5 of 11 patients, but the paper does not establish that Th17 cell numbers were increased in myocardial tissue. Page numbers are unavailable in our copy. (LLM, conf=0.88)
Experimental — accuracy not yet measured
A decreased number of circulating regulatory T cells were found in patients with myocarditis, and adoptive transfer of CD4+ T cells with regulatory T-cell depletion induced fatal myocarditis in mice.
“a decreased number of circulating regulatory T cells were found in patients with myocarditis, and adoptive transfer of CD4 + T cells with regulatory T-cell depletion induced fatal myocarditis in mice”
From Autoimmune Myocarditis, Old Dogs and New Tricks. (2024) · cites this paper as [64]
The Results section reports significantly fewer circulating regulatory T cells in the myocarditis/DCM cohort than in healthy controls. The Introduction separately describes myocarditis induced by transfer of cardiac myosin–stimulated CD4+ T cells, while the Results cite Treg-depleted mice developing myocarditis. Neither passage says that transfer combined with Treg depletion induced fatal myocarditis; the Introduction's lethal outcome concerns a different mouse model. Page numbers were not provided in our copy. (LLM, conf=0.90)
Experimental — accuracy not yet measuredIn patients with myocarditis or idiopathic DCM who tested negative for specific viruses, circulating Th17 cells specific for cardiac myosin in the blood have been reported, along with a reduced number of regulatory T cells.
“In patients with myocarditis or idiopathic DCM who tested negative for specific viruses, the presence of circulating Th17 cells specific for cardiac myosin in the blood has been reported, along with a reduced number of regulatory T cells. 64,238,311”
From Autoimmune Myocarditis, Old Dogs and New Tricks. (2024) · cites this paper as [64]
The Results section on regulatory T cells reports significantly fewer Tregs in peripheral blood, and the Discussion reports elevated Th17 cells in the myocarditis/DCM cohort (page numbers unavailable). However, the paper does not establish that the circulating Th17 cells were cardiac-myosin-specific. The Methods section on patient samples explicitly says viral myocarditis was not determined by PCR or viral culture, so the cohort cannot be described as having tested negative for specific viruses. (LLM, conf=0.90)
Experimental — accuracy not yet measured
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- Authors
- Myers, J. M., Cooper, L. T., Kem, D. C., Stavrakis, S., Kosanke, S. D., Shevach, E. M., Fairweather, D., Stoner, J. A., Cox, C. J., & Cunningham, M. W.
- Affiliations
- University of Oklahoma Health Sciences Center (US)
- Mayo Clinic in Florida (US)
- Department of Medicine/Endocrinology,
- Medicine/Cardiology, and
- National Institutes of Health (US)
- Johns Hopkins University (US)
- Corresponding author
- Cox, Carol J.
- Cunningham, Madeleine W.
- ORCID
- Venue
- JCI Insight
- Published
- 2016-06-16
- Volume
- 1
- Issue
- 9
- ISSN
- 2379-3708 (ISSN-L)
- PMC
- PMC4924810
- OpenAlex
- W2434470226
- Cited by
- 230
- References
- 88
- Citations by year
- 2026: 22 · 2025: 26 · 2024: 33 · 2023: 34 · 2022: 24 · 2021: 29 · 2020: 24 · 2019: 16 · 2018: 12 · 2017: 9 · 2016: 1
- FWCI
- 10.43
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- JCI Insight (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Heart Association (U54GM104938)
- University of Oklahoma
- University of Oklahoma Health Sciences Center
- National Heart, Lung, and Blood Institute (R01HL135165, R56HL056267, R01HL111938, R01HL056267, R37HL035280)
- National Institute of General Medical Sciences (U54GM104938)
- National Institute of Allergy and Infectious Diseases (T32AI007633)
- National Institute of Environmental Health Sciences (R21ES024414)
- 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
- myocarditis, dilated cardiomyopathy, heart failure, Th17 cells, cardiac myosin, TLR2, CD14+ monocytes, IL-17, interleukin-6, TGF-beta, IL-23, GM-CSF, regulatory T cells, Foxp3, autoimmunity
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