期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 208, 期 10, 页码 2005-2016出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20101159
关键词
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资金
- Burroughs Wellcome Fund Translational Research Award
- National Cancer Institute [P01 CA97296]
- University of Chicago
- Medical Science Training Program
Despite lack of tumor control in many models, spontaneous T cell priming occurs frequently in response to a growing tumor. However, the innate immune mechanisms that promote natural antitumor T cell responses are undefined. In human metastatic melanoma, there was a correlation between a type I interferon (IFN) transcriptional profile and T cell markers in metastatic tumor tissue. In mice, IFN-beta was produced by CD11c(+) cells after tumor implantation, and tumor-induced T cell priming was defective in mice lacking IFN-alpha/beta R or Stat1. IFN signaling was required in the hematopoietic compartment at the level of host antigen-presenting cells, and selectively for intratumoral accumulation of CD8 alpha(+) dendritic cells, which were demonstrated to be essential using Batf3(-/-) mice. Thus, host type I IFNs are critical for the innate immune recognition of a growing tumor through signaling on CD8 alpha(+) DCs.
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