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      Batf3 deficiency reveals a critical role for CD8alpha+ dendritic cells in cytotoxic T cell immunity.

      Science (New York, N.Y.)

      blood, immunology, West Nile virus, West Nile Fever, T-Lymphocytes, Cytotoxic, Spleen, physiology, genetics, Repressor Proteins, Mice, Inbred C57BL, Mice, Male, Lymphocyte Activation, Fibrosarcoma, Female, transplantation, Dendritic Cells, Cytotoxicity, Immunologic, Cross-Priming, CD4-Positive T-Lymphocytes, deficiency, Basic-Leucine Zipper Transcription Factors, analysis, Antigens, CD8, Antibodies, Viral, Animals, Adoptive Transfer

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          Abstract

          Although in vitro observations suggest that cross-presentation of antigens is mediated primarily by CD8alpha+ 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 CD8alpha+ 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 CD8alpha+ dendritic cells and cross-presentation in responses to viruses and in tumor rejection.

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          Author and article information

          Journal
          19008445
          2756611
          10.1126/science.1164206

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