Host type I IFN signals are required for antitumor CD8+ T cell responses through CD8{alpha}+ dendritic cells.

Host type I IFN signals are required for antitumor CD8+ T cell responses through CD8{alpha}+ dendritic cells.
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DOI:
10.1084/jem.20101159
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发表时间:
2011-09-26
期刊:
The Journal of experimental medicine
影响因子:
--
通讯作者:
Gajewski TF
Gajewski TF
中科院分区:
其他
文献类型:
--
作者:
Fuertes MB;Kacha AK;Kline J;Woo SR;Kranz DM;Murphy KM;Gajewski TF

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The generation of antitumor CD8+ T cell responses requires type I interferon responsiveness in host antigen-presenting cells 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-β was produced by CD11c+ cells after tumor implantation, and tumor-induced T cell priming was defective in mice lacking IFN-α/βR or Stat1. IFN signaling was required in the hematopoietic compartment at the level of host antigen-presenting cells, and selectively for intratumoral accumulation of CD8α+ 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 CD8α+ DCs.
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