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Science 14 November 2008:
Vol. 322. no. 5904, pp. 1097 - 1100
DOI: 10.1126/science.1164206
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Reports

Batf3 Deficiency Reveals a Critical Role for CD8{alpha}+ Dendritic Cells in Cytotoxic T Cell Immunity

Kai Hildner,1,2 Brian T. Edelson,1 Whitney E. Purtha,3 Mark Diamond,1 Hirokazu Matsushita,1 Masako Kohyama,1,2 Boris Calderon,1 Barbara U. Schraml,1 Emil R. Unanue,1 Michael S. Diamond,1,3 Robert D. Schreiber,1 Theresa L. Murphy,1 Kenneth M. Murphy1,2*

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.

1 Department of Pathology and Immunology, Washington University School of Medicine, 660 South Euclid Avenue, St. Louis, MO 63110, USA.
2 Howard Hughes Medical Institute, Washington University School of Medicine, 660 South Euclid Avenue, St. Louis, MO 63110, USA.
3 Departments of Medicine and Molecular Microbiology, 660 South Euclid Avenue, St. Louis, MO 63110, USA.

* To whom correspondence should be addressed. E-mail: kmurphy{at}wustl.edu

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Science. ISSN 0036-8075 (print), 1095-9203 (online)