The DOI matches its Crossref record; 43 of the 43 references it cites were found in a registry or an index.
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”
From Autoimmune Myocarditis, Old Dogs and New Tricks. (2024) · cites this paper as [98]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“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]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
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“However, this finding was not replicated in other researchers' investigations”
From Autoimmune Myocarditis, Old Dogs and New Tricks. (2024) · cites this paper as [98]
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Citations
Cites
PD-1 and Its Ligands in Tolerance and Immunity
Keir, M. E., Butte, M. J., Freeman, G. J., & Sharpe, A. H. (2008) · Annual Review of Immunology · doi:10.1146/annurev.immunol.26.021607.090331 · Cited by 5,378
Self-citationT cell receptor antagonist peptides induce positive selection.
Hogquist, K., Jameson, S., Heath, W., Howard, J. L., Bevan, M., & Carbone, F. (1994) · Cell · doi:10.1016/0092-8674(94)90169-4 · Cited by 3,252
Brahmer, J. R., Drake, C. G., WOLLNER, I. S., Powderly, J. D., Picus, J., Sharfman, W. H., Stankevich, E., Pons, A., Salay, T. M., McMiller, T. L., et al. (2010) · Journal of Clinical Oncology · doi:10.1200/jco.2009.26.7609 · Cited by 2,967
The PD‐1 pathway in tolerance and autoimmunity
Francisco, L. M., Sage, P. T., & Sharpe, A. H. (2010) · Immunological Reviews · doi:10.1111/j.1600-065x.2010.00923.x · Cited by 2,300
Self-citationTargeting Tim-3 and PD-1 pathways to reverse T cell exhaustion and restore anti-tumor immunity
Sakuishi, K., Apetoh, L., Sullivan, J. M., Blazar, B. R., Kuchroo, V. K., & Anderson, A. C. (2010) · Journal of Experimental Medicine · doi:10.1084/jem.20100643 · Cited by 2,072
Autoimmune Dilated Cardiomyopathy in PD-1 Receptor-Deficient Mice
Nishimura, H., Okazaki, T., Tanaka, Y., Nakatani, K., Hara, M., Matsumori, A., Sasayama, S., Mizoguchi, A., Hiai, H., Minato, N., et al. (2001) · Science · doi:10.1126/science.291.5502.319 · Cited by 1,868
Butte, M. J., Keir, M. E., Phamduy, T. B., Sharpe, A. H., & Freeman, G. J. (2007) · Immunity · doi:10.1016/j.immuni.2007.05.016 · Cited by 1,785
Self-citationSharpe, A. H., & Freeman, G. J. (2002) · Nature reviews. Immunology · doi:10.1038/nri727 · Cited by 1,759
Self-citationTissue expression of PD-L1 mediates peripheral T cell tolerance
Keir, M. E., Liang, S. C., Guleria, I., Latchman, Y. E., Qipo, A., Albacker, L. A., Koulmanda, M., Freeman, G. J., Sayegh, M. H., & Sharpe, A. H. (2006) · The Journal of Experimental Medicine · doi:10.1084/jem.20051776 · Cited by 1,244
Self-citationGood‐Jacobson, K. L., Szumilas, C. G., Chen, L., Sharpe, A. H., Tomayko, M. M., & Shlomchik, M. J. (2010) · Nature Immunology · doi:10.1038/ni.1877 · Cited by 720
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Fulminant Myocarditis with Combination Immune Checkpoint Blockade
Johnson, D. B., Balko, J. M., Compton, M. L., Chalkias, S., Gorham, J., Xu, Y., Hicks, M., Puzanov, I., Alexander, M. R., Bloomer, T. L., et al. (2016) · New England Journal of Medicine · doi:10.1056/nejmoa1609214 · Cited by 2,308
Self-citationLinette, G. P., Stadtmauer, E. A., Maus, M. V., Rapoport, A. P., Levine, B. L., Emery, L., Litzky, L. A., Bagg, A., Carreno, B. M., Cimino, P. J., et al. (2013) · Blood · doi:10.1182/blood-2013-03-490565 · Cited by 1,209
Fundamental Mechanisms of Regulated Cell Death and Implications for Heart Disease
Re, D. P. D., Amgalan, D., Linkermann, A., Liu, Q., & Kitsis, R. N. (2019) · Physiological Reviews · doi:10.1152/physrev.00022.2018 · Cited by 994
Adverse cardiac effects of cancer therapies: cardiotoxicity and arrhythmia
Herrmann, J. (2020) · Nature Reviews Cardiology · doi:10.1038/s41569-020-0348-1 · Cited by 747
Collateral damage: Insulin-dependent diabetes induced with checkpoint inhibitors
Stamatouli, A. M., Quandt, Z., Perdigoto, A. L., Clark, P. L., Kluger, H., Weiss, S. A., Gettinger, S., Sznol, M., Young, A., Rushakoff, R., et al. (2018) · Diabetes · doi:10.2337/dbi18-0002 · Cited by 590
Metadata
- 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 › 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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