Differential regulation of CD8+ T cell senescence in mice and men |
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| Affiliation: | 1. Department of Medicine, Division of Hematology/Oncology, University of California at Irvine, Irvine, CA 92697, USA;2. Department of Biological Chemistry, University of California at Irvine, Irvine, CA 92697, USA;3. School of Biological Sciences, University of California at Irvine, Irvine, CA 92697, USA;4. Chao Family Comprehensive Cancer Center, University of California at Irvine, Irvine, CA 92697, USA;1. Department of neurology, The Affiliated YanAn Hospital of Kunming Medical University, Kunming, 650051, Yunnan, China;2. Department of Gastroenterology, The Affiliated YanAn Hospital of Kunming Medical University, Kunming, 650051, Yunnan, China;3. Department of General Surgery, The Affiliated YanAn Hospital of Kunming Medical University, Kunming, 650051, Yunnan, China;2. Key Laboratory of Tumor Immunological Prevention and Treatment of Yunnan Province, China |
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| Abstract: | The cytotoxic CD8+ T cell population expands considerably during acute immune infection with virus. Most of these cells are removed by apoptosis at the end of the immune response. However, a balance has to be attained between clearance and retention of a memory population of cells, which respond more rapidly and efficiently to secondary encounter with the antigen. In this article, the role of apoptosis and in particular the development of replicative senescence as mechanisms which control this homeostatic balance are discussed. Although similar mechanisms regulate apoptosis in both humans and rodents, the available data suggests that replicative senescence may be controlled differently in these species, suggesting the there may be different constraints in the regulation of CD8+ T cell memory between different species. |
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