期刊
BLOOD CELLS MOLECULES AND DISEASES
卷 27, 期 1, 页码 223-230出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1006/bcmd.2001.0379
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资金
- NATIONAL CANCER INSTITUTE [R37CA068458, T32CA009498, R01CA065670, R01CA068458, P30CA016058] Funding Source: NIH RePORTER
- NCI NIH HHS [T32 CA-09498, CA-68458, P30CA-16058, CA-65670] Funding Source: Medline
The role of inflammation in the early genesis of certain malignancies has recently been appreciated. Interleukin (IL)-15, a proinflammatory cytokine and growth factor, is required for lymphocyte homeostasis. Intriguingly, the expression of IL-15 protein is tightly controlled by multiple posttranscriptional mechanisms, suggesting that inappropriate expression of IL-15 may be detrimental to the host. We recently engineered a transgenic mouse in which the normal posttranscriptional control of IL-15 is eliminated, thereby overexpressing the murine IL-15 protein. IL-15 transgenic mice have early expansions in NK and CD8(+) T lymphocytes and later develop fatal lymphocytic leukemia with a T-NK phenotype. This article recapitulates the phenotype of these IL-15 transgenic mice and discusses the utility of this model as a tool to further our understanding of leukemogenesis. (C) 2001 Academic Press.
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