@article {542376,
	title = {T-cell costimulation and coinhibition in atherosclerosis.},
	journal = {Circ Res},
	volume = {103},
	number = {11},
	year = {2008},
	month = {2008 Nov 21},
	pages = {1220-31},
	abstract = {Evidence from many human and rodent studies has established that T lymphocytes enhance inflammation in atherosclerotic plaques and contribute to lesion progression and remodeling. Recent work also indicates that regulatory T cells are important in limiting proatherogenic T-cell responses. Given the important role of T cells in atherosclerosis, there is a need to fully understand how proatherogenic T cells are activated and regulated. Antigen-dependent activation of na{\"\i}ve T cells, leading to clonal expansion and effector T-cell differentiation, and effector and memory T cells, is enhanced by signals provided by costimulatory molecules expressed by antigen presenting cells, which bind to receptors on the T cells. In addition, T-cell responses to antigen are negatively regulated by coinhibitory molecules expressed by antigen-presenting cells, which bind to receptors on T cells. Two major families of costimulatory molecules include the B7 and the tumor necrosis factor (TNF) families. These molecules bind to receptors on T cells belonging to the CD28 or TNF receptor families, respectively. The best-defined coinhibitors and their receptors belong to the B7 and CD28 families. Recent work has begun to define how these T-cell costimulatory and coinhibitory pathways influence atherosclerosis, largely in mouse models of the disease. Profound effects are attributable to molecules in both the B7/CD28 (B7-1/2, ICOS, and PDL-1/2) and the TNF/TNF receptor (CD40, OX40, and CD137) families. One emerging theme is that both pathogenic effector T-cell responses and regulatory T cells are influenced by overlapping sets of costimulators and coinhibitors. These complexities must be considered as immunotherapeutic approaches for atherosclerotic disease are developed.},
	keywords = {Animals, Antigens, CD, Antigens, CD28, Atherosclerosis, CD40 Ligand, Cell Differentiation, Humans, Immunologic Memory, Immunotherapy, Lymphocyte Activation, Major Histocompatibility Complex, Mice, Models, Animal, Receptors, Antigen, T-Cell, T-Lymphocytes, T-Lymphocytes, Regulatory, Tumor Necrosis Factor-alpha},
	issn = {1524-4571},
	doi = {10.1161/CIRCRESAHA.108.182428},
	author = {Gotsman, Israel and Sharpe, Arlene H and Lichtman, Andrew H}
}
