TY - JOUR
T1 - Fatal leukemia in interleukin-15 transgenic mice
AU - Fehniger, Todd A.
AU - Suzuki, Kazuhiro
AU - VanDeusen, Jeffrey B.
AU - Cooper, Megan A.
AU - Freud, Aharon G.
AU - Caligiuri, Michael A.
N1 - Funding Information:
This work was supported by Grants CA-68458, CA-65670, and P30CA-16058 from the National Institutes of Health. T. A. Fehniger is the recipient of Medical Scientist Program (MSP) and Bennett Fellowships from the Ohio State University College of Medicine. J. B. Van-Deusen is supported by T-32 CA-09498 and M. A. Cooper by the HHMI Medical Student Research Fellowship. This paper was presented at a Focused Workshop on Animal Models of Leukemia and Lymphoma jointly sponsored by the Leukemia & Lymphoma Society and the Mouse Models of Human Cancer Consortium of the National Cancer Institute on September 19 –20, 2000.
PY - 2001
Y1 - 2001
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=0035046525&partnerID=8YFLogxK
U2 - 10.1006/bcmd.2001.0379
DO - 10.1006/bcmd.2001.0379
M3 - Article
C2 - 11358383
AN - SCOPUS:0035046525
SN - 1079-9796
VL - 27
SP - 223
EP - 230
JO - Blood Cells, Molecules, and Diseases
JF - Blood Cells, Molecules, and Diseases
IS - 1
ER -