期刊
JOURNAL OF IMMUNOLOGY
卷 173, 期 6, 页码 3594-3598出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.173.6.3594
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资金
- NIAID NIH HHS [R01AI45860, R01AI59827] Funding Source: Medline
- NIDDK NIH HHS [T32DK60414] Funding Source: Medline
NK cells protect hosts against viral pathogens and transformed cells, and dendritic cells (DCs) play important roles inactivating NK cells. We now find that murine IL15Ralpha-deficient DCs fail to support NK cell cytolytic activity and elaboration of IFN-gamma, despite the fact that these DCs express normal levels of costimulatory molecules and IL-12. By contrast, IL-15Ralpha expression on NK cells is entirely dispensible for their activation by DCs. In addition, blockade with anti-IL-15Ralphaandanti-IL-2Rbeta butnotanti-IL-2Ralpha-specific Abs prevents NK cell activation by wildtype DO. Finally, presentation of IL-15 by purified IL15Ralpha/Fc in trans synergizes with IL-12 to support NK cell priming. These findings suggest that murine DCs require IL-15Ralpha to present IL-15 in trans to NKcells during NK cell priming.
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