@article {542166,
	title = {PD-1 protects against inflammation and myocyte damage in T cell-mediated myocarditis.},
	journal = {J Immunol},
	volume = {188},
	number = {10},
	year = {2012},
	month = {2012 May 15},
	pages = {4876-84},
	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.},
	keywords = {Amino Acid Sequence, Animals, Cell Movement, Cells, Cultured, Coculture Techniques, Disease Models, Animal, Female, Inflammation, Male, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Knockout, Mice, Transgenic, Molecular Sequence Data, Muscle Cells, Myocarditis, Programmed Cell Death 1 Receptor, T-Lymphocyte Subsets},
	issn = {1550-6606},
	doi = {10.4049/jimmunol.1200389},
	author = {Tarrio, Margarite L and Grabie, Nir and Bu, De-xiu and Sharpe, Arlene H and Lichtman, Andrew H}
}
