PD-1 Protects against Inflammation and Myocyte Damage in T Cell-Mediated Myocarditis
Open accessAbstract
PD-1, a member of the CD28 family of immune regulatory molecules, is expressed on activated T cells, interacts with its ligands, PD-L1/B7-H1 and PD-L2/B7-DC, on other cells, and delivers inhibitory signals to the T cell. We studied the role of this pathway in modulating autoreactive T cell responses in two models of myocarditis. In a CD8+ T cell-mediated adoptive transfer model, we found that compared with Pd1+/+ CD8+ T cells, Pd1−/− CD8+ T cells cause enhanced disease, with increased inflammatory infiltrate, particularly rich in neutrophils. Additionally, we show enhanced proliferation in vivo and enhanced cytotoxic activity of PD-1–deficient T lymphocytes against myocardial endothelial cells in vitro. In experimental autoimmune myocarditis, a disease model dependent on CD4+ T cells, we show that mice lacking PD-1 develop enhanced disease compared with wild-type mice. PD-1–deficient mice displayed increased inflammation, enhanced serum markers of myocardial damage, and an increased infiltration of inflammatory cells, including CD8+ T cells. Together, these studies show that PD-1 plays an important role in limiting T cell responses in the heart.
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This finding was not recapitulated in a separately generated PD-1 genetic knockout mouse model in a BALB/c background.
“this finding was not recapitulated in a separately generated PD-1 genetic knockout mouse model in a BALB/c background”
From Autoimmune Myocarditis, Old Dogs and New Tricks. (2024) · cites this paper as [98]
Materials & Methods (Animal Studies; page unavailable) confirms that the paper used PD-1 knockout mice on a BALB/c background. But the paper does not say that a prior finding was not recapitulated in those mice: the Introduction reports prior spontaneous dilated cardiomyopathy in BALB/c PD-1-deficient mice, while the Results describe increased pathology after experimentally induced myocarditis. (LLM, conf=0.86)
Experimental — accuracy not yet measuredAnti-cTnI IgG levels were not significantly elevated in the ICI myocarditis mouse model induced with anti-PD-1 antibody treatment.
“anti-cTnI IgG levels were not significantly elevated in the ICI myocarditis mouse model induced with anti-PD-1 antibody treatment.”
From Autoimmune Myocarditis, Old Dogs and New Tricks. (2024) · cites this paper as [98]
The Materials & Methods section ('Serum troponis determinations'; page not provided) measures circulating cardiac troponin I, not anti-cTnI IgG. The myocarditis-induction methods describe transfer of PD-1-deficient T cells rather than anti-PD-1 antibody treatment. Searches for anti-cTnI IgG and anti-PD-1 antibody treatment found no result addressing the claimed antibody levels. (LLM, conf=0.76)
Experimental — accuracy not yet measuredThe finding of anti-cTnI antibody cardiotoxicity was not replicated in other researchers' investigations.
“However, this finding was not replicated in other researchers' investigations”
From Autoimmune Myocarditis, Old Dogs and New Tricks. (2024) · cites this paper as [98]
The References section lists a study attributing cardiomyopathy to anti-cTnI autoantibodies, but does not say whether other investigators replicated that finding. The Discussion and Results address PD-1-related heart injury, not attempts to reproduce antibody cardiotoxicity (searched: replicated, autoantibodies, and failed reproduction). (LLM, conf=0.74)
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- Authors
- Tarrio, M. L., Grabie, N., Bu, D.-X., Sharpe, A. H., & Lichtman, A. H.
- Affiliations
- Brigham and Women's Hospital (US)
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2012-05
- Volume
- 188
- Issue
- 10
- Pages
- 4876-4884
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- PMC
- PMC3345066
- OpenAlex
- W2130852062
- Semantic Scholar
- 25f4092ea5db9b9d9a0f493ce69a14946198bed4
- Cited by
- 288
- References
- 43
- Citations by year
- 2026: 20 · 2025: 21 · 2024: 27 · 2023: 24 · 2022: 31 · 2021: 32 · 2020: 29 · 2019: 26 · 2018: 26 · 2017: 21 · 2016: 12 · 2015: 5 · 2014: 5 · 2013: 6 · 2012: 3
- FWCI
- 3.86
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Brigham and Women's Hospital
- National Institutes of Health (HL‐36028, HL56985)
- National Heart, Lung, and Blood Institute (P50HL056985, R01 HL36028, P01HL036028, R01HL087282)
- National Institute of Allergy and Infectious Diseases (R01AI040614, P01AI056299)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Viral Infections and Immunology Research
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Keywords
- PD-1, PD-L1, PD-L2, experimental autoimmune myocarditis, adoptive transfer, CD8+ T cells, CD4+ T cells, myocarditis, myocardial injury, neutrophils, T cell proliferation, cytotoxicity, immune checkpoint
- MeSH terms
- Amino Acid Sequence, Animals, Cell Movement, Cells, Cultured, Disease Models, Animal, Female, Inflammation, Male, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Transgenic, Molecular Sequence Data, Myocarditis, T-Lymphocyte Subsets, Mice, Knockout, Coculture Techniques, Muscle Cells, Mice, Programmed Cell Death 1 Receptor
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