Batf3 Deficiency Reveals a Critical Role for CD8α+ Dendritic Cells in Cytotoxic T Cell Immunity

被引:1545
作者
Hildner, Kai [1 ,2 ]
Edelson, Brian T. [1 ]
Purtha, Whitney E. [3 ,4 ]
Diamond, Mark [1 ]
Matsushita, Hirokazu [1 ]
Kohyama, Masako [1 ,2 ]
Calderon, Boris [1 ]
Schraml, Barbara U. [1 ]
Unanue, Emil R. [1 ]
Diamond, Michael S. [1 ,3 ,4 ]
Schreiber, Robert D. [1 ]
Murphy, Theresa L. [1 ]
Murphy, Kenneth M. [1 ,2 ]
机构
[1] Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO 63110 USA
[2] Washington Univ, Sch Med, Howard Hughes Med Inst, St Louis, MO 63110 USA
[3] Washington Univ, Sch Med, Dept Med, St Louis, MO 63110 USA
[4] Washington Univ, Sch Med, Dept Mol Microbiol, St Louis, MO 63110 USA
关键词
D O I
10.1126/science.1164206
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Although in vitro observations suggest that cross- presentation of antigens is mediated primarily by CD8 alpha(+) dendritic cells, in vivo analysis has been hampered by the lack of systems that selectively eliminate this cell lineage. We show that deletion of the transcription factor Batf3 ablated development of CD8 alpha(+) dendritic cells, allowing us to examine their role in immunity in vivo. Dendritic cells from Batf3(-/-) mice were defective in cross- presentation, and Batf3(-/-) mice lacked virus- specific CD8(+) T cell responses to West Nile virus. Importantly, rejection of highly immunogenic syngeneic tumors was impaired in Batf3(-/-) mice. These results suggest an important role for CD8 alpha(+) dendritic cells and cross- presentation in responses to viruses and in tumor rejection.
引用
收藏
页码:1097 / 1100
页数:4
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