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Brief Definitive Reports

Interleukin 12–dependent Interferon Production by CD8⁺Lymphoid Dendritic Cells

Toshiaki Ohteki^*, Taro Fukao^*, Kazutomo Suzue^*, Chikako Maki^*, Mamoru Ito, Masataka Nakamura, and Shigeo Koyasu^*

From the ^* Department of Immunology, Keio University School of Medicine, Shinjuku-ku, Tokyo 160-8582, Japan; the Laboratory of Immunology, Central Institute for Experimental Animals, Kawasaki 216-0001, Japan; and the Human Gene Sciences Center, Tokyo Medical and Dental University, Bunkyo-ku, Tokyo 113, Japan

We investigated the role of antigen-presenting cells in early interferon (IFN)- production in normal and recombinase activating gene 2–deficient (Rag-2^–/–) mice in response to Listeria monocytogenes (LM) infection and interleukin (IL)-12 administration. Levels of serum IFN- in Rag-2^–/– mice were comparable to those of normal mice upon either LM infection or IL-12 injection. Depletion of natural killer (NK) cells by administration of anti-asialoGM1 antibodies had little effect on IFN- levels in the sera of Rag-2^–/– mice after LM infection or IL-12 injection. Incubation of splenocytes from NK cell–depleted Rag-2^–/– mice with LM resulted in the production of IFN- that was completely blocked by addition of anti–IL-12 antibodies. Both dendritic cells (DCs) and monocytes purified from splenocytes were capable of producing IFN- when cultured in the presence of IL-12. Intracellular immunofluorescence analysis confirmed the IFN- production from DCs. It was further shown that IFN- was produced predominantly by CD8⁺ lymphoid DCs rather than CD8^– myeloid DCs. Collectively, our data indicated that DCs are potent in producing IFN- in response to IL-12 produced by bacterial infection and play an important role in innate immunity and subsequent T helper cell type 1 development in vivo.

Key Words: recombinase-activating gene 2 knockout mouse • nonobese diabetic-severe combined immunodeficiency disease mouse • _c knockout mouse • natural killer cells • Listeria monocytogenes

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