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JCI online early table of contents: Feb. 7, 2008

ivated pDCs directly into one of the tumors. Importantly, the tumor-specific CD8+ T cell immune response was not limited to the tumor into which the TLR9-activated pDCs had been injected. The TLR9-activated pDCs were shown to induce this antitumor immune response by recruiting and activating NK cells, which, in turn, activated cDCs, enabling them to activate tumor-specific CD8+ T cells. These data have provided insight into a cascade of immune cell activation that can result in antitumor immune responses, information that might lead to the development of new therapeutic antitumor approaches.

TITLE: Plasmacytoid dendritic cells induce NK celldependent, tumor antigenspecific T cell cross-priming and tumor regression in mice

Patrick Hwu
The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Phone: (713) 563-1727; Fax: (713) 745-1046; E-mail:

Gang Wang
US Food and Drug Administration, Rockville, Maryland, USA.
Phone: (301) 827-7123; Fax: (301) 827-3536; E-mail:

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IMMUNOLOGY: T cells stopped from reaching their destination

If immune cells known as T cells are to mount an effective immune response they must be able to migrate to and be retained in the tissue where the immune response is needed. New data, generated in mice by Federica Marelli-Berg and colleagues at Imperial College London, United Kingdom, have indicated that signaling through the protein PI3K p110-delta is important for T cells to localize in tissues where they are needed to mount an immune response.

In the study, when T cells from mice expressing an inactive form of PI3K p110-delta were transferred to normal mi

Contact: Karen Honey
Journal of Clinical Investigation

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