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Role for IL-15/IL-15 receptor beta-chain in natural killer 1.1+ T cell receptor-alpha beta+ cell development
1Department of Medical Biophysics, Ontario Cancer Institute, Toronto, Canada.
Mouse TCR alphabeta+ cells expressing NKR-P1 (NK1+ T cells in the C57BL/6 strain) are classified as a unique subset that require beta2m-associated, MHC class I-like molecules for development and preferentially express particular V beta and V alphaJ domains of the TCR. We show here that NK1+ T cells express the IL-2R beta/IL-15R beta that is normally present on conventional NK cells, but not T cells. In mice lacking IL-2R beta/IL-15R beta chain, the number of NK1+ T cells is dramatically reduced. However, in IL-2-deficient mice, NK1+ T cells develop normally. Moreover, NK1+ T cells proliferate upon stimulation by IL-15, and the proliferation is blocked by the addition of anti-IL-2R beta/IL-15R beta Abs. Collectively, our data indicate that NK1+ T cells require IL-2R beta/IL-15R beta chain in an IL-2-independent manner and demonstrate that IL-15 plays a crucial role during development.
Mouse TCR alphabeta+ cells expressing NKR-P1 (NK1+ T cells in the C57BL/6 strain) are classified as a unique subset that require beta2m-associated, MHC class I-like molecules for development and preferentially express particular V beta and V alphaJ domains of the TCR. We show here that NK1+ T cells express the IL-2R beta/IL-15R beta that is normally present on conventional NK cells, but not T cells. In mice lacking IL-2R beta/IL-15R beta chain, the number of NK1+ T cells is dramatically reduced. However, in IL-2-deficient mice, NK1+ T cells develop normally. Moreover, NK1+ T cells proliferate upon stimulation by IL-15, and the proliferation is blocked by the addition of anti-IL-2R beta/IL-15R beta Abs. Collectively, our data indicate that NK1+ T cells require IL-2R beta/IL-15R beta chain in an IL-2-independent manner and demonstrate that IL-15 plays a crucial role during development.
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