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© The Rockefeller University Press, 0022-1007/1998/12/2067/ $5.00
The Journal of Experimental Medicine, Volume 188, Number 11, December 7, 1998 2067-2074

Articles

Stat5b Is Essential for Natural Killer Cell–mediated Proliferation and Cytolytic Activity

Kazunori Imada*, Eda T. Bloom{ddagger}, Hiroshi Nakajima*, Judith A. Horvath-Arcidiacono{ddagger}, Garry B. Udy§, Helen W. Davey, and Warren J. Leonard*

From the * Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892-1674; the {ddagger} Division of Cell and Gene Therapy, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, Maryland 20892; the § Ministry of Agriculture and Forestry (Verification Agency), Te Kuiti, New Zealand; and the Dairy Science Group, AgResearch, Ruakura, Hamilton, New Zealand

We have analyzed the immune system in Stat5-deficient mice. Although Stat5a–/– splenocytes have a partial defect in anti-CD3-induced proliferation that can be overcome by high dose interleukin (IL)-2, we now demonstrate that defective proliferation in Stat5b–/– splenocytes cannot be corrected by this treatment. Interestingly, this finding may be at least partially explained by diminished expression of the IL-2 receptor β chain (IL-2Rβ), which is a component of the receptors for both IL-2 and IL-15, although other defects may also exist. Similar to the defect in proliferation in activated splenocytes, freshly isolated splenocytes from Stat5b–/– mice exhibited greatly diminished proliferation in response to IL-2 and IL-15. This results from both a decrease in the number and responsiveness of natural killer (NK) cells. Corresponding to the diminished proliferation, basal as well as IL-2– and IL-15–mediated boosting of NK cytolytic activity was also greatly diminished. These data indicate an essential nonredundant role for Stat5b for potent NK cell–mediated proliferation and cytolytic activity.

Key Words: natural killer cells • Stat5b • Stat5a • interleukin 2 • interleukin 15

Address correspondence to Warren J. Leonard, Bldg. 10, Rm. 7N252, NIH, Bethesda, MD 20892-1674. Phone: 301-496-0098; Fax: 301-402-0971; E-mail: wjl{at}helix.nih.gov

K. Imada was supported in part by a Japanese Society for the Promotion of Science research fellowship for Japanese biomedical and behavioral researchers at NIH and by the Sankyo Foundation of Life Science.

Abbreviations used: STAT, signal transducers and activators of transcription.


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