Asset Details
Do you wish to reserve the book?
The epitranscriptional factor PCIF1 orchestrates CD8+ T cell ferroptosis and activation to control antitumor immunity
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
The epitranscriptional factor PCIF1 orchestrates CD8+ T cell ferroptosis and activation to control antitumor immunity
Do you wish to request the book?
The epitranscriptional factor PCIF1 orchestrates CD8+ T cell ferroptosis and activation to control antitumor immunity
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
The epitranscriptional factor PCIF1 orchestrates CD8+ T cell ferroptosis and activation to control antitumor immunity
2025
Overview
T cell-based immunotherapies have revolutionized cancer treatment, yet durable responses remain elusive. Here we show that PCIF1, an RNA
N
6
2′-
O
-dimethyladenosine (m
6
A
m
) methyltransferase, negatively regulates CD8
+
T cell antitumor responses. Whole-body or T cell-specific
Pcif1
knockout (KO) reduced tumor growth in mice. Single-cell RNA sequencing shows an increase in the number of tumor-infiltrating cytotoxic CD8
+
T cells in
Pcif1
-deficient mice. Mechanistically, proteomic and m
6
A
m
-sequencing analyses pinpoint that
Pcif1
KO elevates m
6
A
m
-modified targets, specifically ferroptosis suppressor genes (
Fth1
,
Slc3a2
), and the T cell activation gene
Cd69
, imparting resistance to ferroptosis and enhancing CD8
+
T cell activation. Of note,
Pcif1
-deficient mice had enhanced responses to anti-PD-1 immunotherapy, and
Pcif1
KO chimeric antigen receptor T cells improved tumor control. Clinically, cancer patients with low PCIF1 expression in T cells have enhanced responses to immunotherapies. These findings suggest that PCIF1 suppresses CD8
+
T cell activation and targeting PCIF1 is a promising strategy to boost antitumor immunity.
Here the authors show that PCIF1 can regulate CD8
+
T cell antitumor responses in mice and use this information to enhance chimeric antigen receptor T cell design.
Publisher
Nature Publishing Group US,Nature Publishing Group
Subject
/ Animals
/ Antigens
/ Antigens, Differentiation, T-Lymphocyte - genetics
/ Antigens, Differentiation, T-Lymphocyte - metabolism
/ Biomedical and Life Sciences
/ CD8-Positive T-Lymphocytes - immunology
/ Humans
/ Immunity
/ Lectins, C-Type - metabolism
/ Lymphocyte Activation - immunology
/ Lymphocytes, Tumor-Infiltrating - immunology
/ Methyltransferases - genetics
/ Methyltransferases - immunology
/ Methyltransferases - metabolism
/ Mice
