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IFNγ signaling in cytotoxic T cells restricts anti-tumor responses by inhibiting the maintenance and diversity of intra-tumoral stem-like T cells

Abstract:

IFNγ is an immune mediator with concomitant pro- and anti-tumor functions. Here, we provide evidence that IFNγ directly acts on intra-tumoral CD8 T cells to restrict anti-tumor responses. We report that expression of the IFNγ receptor β chain (IFNγR2) in CD8 T cells negatively correlates with clinical responsiveness to checkpoint blockade in metastatic melanoma patients, suggesting that the loss of sensitivity to IFNγ contributes to successful antitumor immunity. Indeed, specific deletion of ...

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Publication status:
Published
Peer review status:
Peer reviewed

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Publisher copy:
10.1038/s41467-023-35948-9

Authors


More by this author
Institution:
University of Oxford
Division:
MSD
Department:
NDORMS
Sub department:
Kennedy Institute for Rheumatology
Role:
Author
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
NDORMS
Sub department:
Kennedy Institute for Rheumatology
Role:
Author
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
Oncology
Role:
Author
ORCID:
0000-0002-0659-5944
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
Oncology
Role:
Author
ORCID:
0000-0002-8838-9406
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
NDORMS
Sub department:
Kennedy Institute for Rheumatology
Role:
Author
ORCID:
0000-0001-5546-9752
More from this funder
Name:
Cancer Research UK
Grant:
29549
More from this funder
Name:
Kennedy Trust for Rheumatology Research
Grant:
KENN 20 21 12
More from this funder
Name:
Biotechnology and Biological Sciences Research Council
Grant:
BB/R015651/1
Publisher:
Springer Nature
Journal:
Nature Communications More from this journal
Volume:
14
Issue:
1
Article number:
321
Publication date:
2023-01-19
Acceptance date:
2023-01-10
DOI:
EISSN:
2041-1723
Language:
English
Keywords:
Pubs id:
1324509
Local pid:
pubs:1324509
Deposit date:
2023-01-19

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