- Abstract:
-
Treatment of tumors with ionizing radiation stimulates an antitumor immune response partly dependent on induction of IFNs. These IFNs directly enhance dendritic cell and CD8+ T cell activity. Here we show that resistance to an effective antitumor immune response is also a result of IFN signaling in a different cellular compartment of the tumor, the cancer cells themselves. We abolished type I IFN signaling in cancer cells by genetic elimination of its receptor, IFNAR1. Pronounced immune respo...
Expand abstract - Publication status:
- Published
- Peer review status:
- Peer reviewed
- Files:
-
-
(, 0.0b)
-
- Publisher copy:
- 10.1172/JCI127458
-
Version unsuitable
-
We have not obtained a suitable full-text for a given research output. See this page for more information.
-
Recently completed
-
Sometimes content is held in ORA but is unavailable for a fixed period of time to comply with the policies and wishes of rights holders.
-
Permissions
-
All content made available in ORA should comply with relevant rights, such as copyright. See this page for more information.
-
Clearance
-
Some thesis volumes scanned as part of the digitisation scheme funded by Dr Leonard Polonsky are currently unavailable due to sensitive material or uncleared third-party copyright content. We are attempting to contact authors whose theses are affected.
- Publisher:
- American Society for Clinical Investigation Publisher's website
- Journal:
- Journal of Clinical Investigation Journal website
- Volume:
- 129
- Issue:
- 10
- Pages:
- 4224-4238
- Publication date:
- 2019-10-01
- Acceptance date:
- 2019-07-03
- DOI:
- EISSN:
-
1558-8238
- ISSN:
-
0021-9738
- Pmid:
-
31483286
- Pubs id:
-
1049655
- Local pid:
- pubs:1049655
- Language:
- English
- Keywords:
- Format:
- Copyright holder:
- Chen et al.
- Copyright date:
- 2019
- Rights statement:
- © 2019 Chen, et al. This is an open access article published under the terms of the Creative Commons Attribution 4.0 International License.
- License:
- CC Attribution (CC BY)
Journal article
Type I IFN protects cancer cells from CD8+ T cell-mediated cytotoxicity after radiation
Actions
Access Document
Why is the content I wish to access not available via ORA?
Bibliographic data (the information relating to research outputs) and full-text items (e.g. articles, theses, reports, etc.) arrive in ORA from several different sources. Unfortunately we are not able to make available the full-text for every research output.
Please contact the ORA team (
) if you have queries regarding unavailable content OR if you are aware of a full-text copy we can make available.
) if you have queries regarding unavailable content OR if you are aware of a full-text copy we can make available.
Content may be unavailable for the following four reasons
Alternative access to the full-text
You may be able to access the full-text directly from the publisher's website using the 'Publisher Copy' link in the 'Links & Downloads' box from a research output's ORA record page. This method may require an institutional or individual subscription to the journal/resource.
Authors
Funding
Bibliographic Details
Item Description
Terms of use
Metrics
Altmetrics
Dimensions
If you are the owner of this record, you can report an update to it here: Report update to this record