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The Journal of Immunology, 2004, 173: 4218-4229.
Copyright © 2004 by The American Association of Immunologists

CD137-Deficient Mice Have Reduced NK/NKT Cell Numbers and Function, Are Resistant to Lipopolysaccharide-Induced Shock Syndromes, and Have Lower IL-4 Responses1

Dass S. Vinay*, Beom K. Choi*,{dagger}, Jun S. Bae*,{dagger}, Won Y. Kim*,{dagger}, Bryan M. Gebhardt* and Byoung S. Kwon2,*,{dagger}

* Louisiana State University Eye Center, Louisiana State University Health Sciences Center School of Medicine, New Orleans, LA 70112; and {dagger} Immunomodulation Research Center and Department of Biological Sciences, University of Ulsan, Ulsan, Korea

CD137, a member of the TNF superfamily, is involved in T cell and NK cell activation and cytokine production. To establish its in vivo role in systems dependent on NK and NKT cells, we studied the response of CD137–/– mice to LPS-induced shock, tumor killing, and their IL-4-controlled Th2 responses. In both high and low dose shock models, all the CD137-deficient mice, but none of the wild-type BALB/c mice, survived. After injection of LPS/2-amino-2-deoxy-D-galactose (D-gal), CD137–/– mice had reduced serum cytokine levels and substantially impaired liver IFN-{gamma} and TNF-{alpha} mRNA levels. Phenotypic analysis of mononuclear cells revealed fewer NK and NKT cells in the CD137–/– mice. The knockout mice did not generate a rapid IL-4 response after systemic T cell activation, or effective Ag-specific Th2 responses. In addition, both in vitro and in vivo NK-specific cytolytic activities were reduced. These findings suggest that CD137-directed NK/NKT cells play an important role in the inflammatory response leading to the production of proinflammatory cytokines, LPS-induced septic shock, and tumor killing, as well as IL-4-dependent Th2 responses.




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