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lüll Immunoregulatory role of B7-H1 in chronicity of inflammatory responses Dong H; Chen XCell Mol Immunol 2006[Jun]; 3 (3): 179-87Pathogenesis of most chronic human diseases, including chronic infections, autoimmune diseases and cancers, often involves a persistent, unresolved inflammatory response. The molecular mechanisms that determine the conversion of an acute inflammatory response into a chronic process had puzzled researchers for many years. Recent studies reveal that B7-H1 (CD274, PD-L1), a newly identified co-stimulatory molecule, possesses dual functions of co-stimulation of naive T cells and inhibition of activated effector T cells. The aberrant cellular expression and deregulated function of B7-H1 have been reported during chronic viral and intracellular bacterial infection, as well as in many autoimmune diseases and cancers. Importantly, the deregulation of B7-H1's dual functions appears to be associated with a prolonged and incomplete immune response by luring naive T cells for activation and dampening activated effector T cells. Moreover, development of strategies targeting B7-H1 signals provides a new and promising approach to manipulate the devastating diseases associated with chronic inflammation. Thus, B7-H1 may play a critical immunoregulatory role in the chronicity of inflammatory responses.|*Inflammation/immunology[MESH]|Animals[MESH]|Antigens, CD/*physiology[MESH]|Autoimmunity[MESH]|B7-H1 Antigen[MESH]|Bacterial Infections/*immunology[MESH]|Chronic Disease[MESH]|Humans[MESH]|Neoplasms/*immunology[MESH]|Virus Diseases/*immunology[MESH] |