Cited by 288Viral Infections and Immunology ResearchT-cell and B-cell ImmunologyCardiac Fibrosis and Remodeling

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PD-1 Protects against Inflammation and Myocyte Damage in T Cell-Mediated Myocarditis

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Tarrio, Margarite L, Grabie, Nir, Bu, De-xiu, Sharpe, Arlene H, Lichtman, Andrew H·2012·The Journal of Immunology

DOI 10.4049/jimmunol.1200389PMC PMC3345066

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Abstract

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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Authors: Tarrio, M. L., Grabie, N., Bu, D.-X., Sharpe, A. H., & Lichtman, A. H.
Affiliations: Brigham and Women's Hospital (US)
ORCID: Bu, De-xiu
Sharpe, Arlene H
Lichtman, Andrew H
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
DOI: 10.4049/jimmunol.1200389
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
Licence: academic.oup.com/pages/standard-publication-reuse-rights (vor)
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 › Infectious Diseases › 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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PD-1 Protects against Inflammation and Myocyte Damage in T Cell-Mediated Myocarditis

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