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Intracellular Signals of T Cell Costimulation

查看全文 作  者:Fengyang Tylan [1]Lei;Rizwanul [1]Haque 高影响力作者 机构地区:[1]Department of Microbiology and Immunology and Penn State Cancer Institute,the Pennsylvania State University College of Medicine,500 University Dr,Hershey,PA 17033,USA高影响力机构 出  处:《Cellular & Molecular Immunology》索引2008年第5卷第4期,共9页高影响力期刊 基  金:The project was funded,in part,under grants from the Pennsylvania Department of Health and St.Baldrick's Foundation (J.Song) 摘  要:Ligation of T cell receptor (TCR) alone is insufficient to induce full activation of T lymphocytes. Additional ligand-receptor interactions (costimulation) on antigen presenting cells (APCs) and T cells are required. T cell costimulation has been shown to be essential for eliciting efficient T cell responses,involving all phases during T cell development. However,the mechanisms by which costimulation affects the function of T cells still need to be elucidated. In recent years,advances have been made in studies of costimulation as potential therapies in cancer,infectious disease as well as autoimmune disease. In this review,we discussed intracellular costimulation signals that regulate T cell proliferation,cell cycle progression,cytokine production,survival,and memory development. In general,the pathway of phosphoinositide-3 kinase (PI3K)/protein kinase B (PKB,also known as Akt)/nuclear factor κB (NF-κB) might be central to many costimulatory effects. Through these pathways,costimulation controls T-cell expansion and proliferation by maintenance of survivin and aurora B expression,and sustains long-term T-cell survival and memory development by regulating the expression of bcl-2 family members. 关 键 词:细胞受体 信号转换 抗原反应细胞 T细胞发展
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