Rejuvenating dysfunctional T cells in ovarian cancer: CD28 is the license to kill
- PMID: 34739843
- DOI: 10.1016/j.ccell.2021.10.011
Rejuvenating dysfunctional T cells in ovarian cancer: CD28 is the license to kill
Abstract
High-grade serous ovarian cancers (HGSOCs) exhibit limited response to immune checkpoint blockade. In a new study in Cancer Cell, Duraiswamy et al. highlight intratumoral CD28 co-stimulation by myeloid-antigen-presenting cells as a key mechanism required for activation of programmed cell death receptor 1 (PD-1)+ tumor-infiltrating T lymphocytes during PD-1 blockade in HGSOC.
Copyright © 2021 Elsevier Inc. All rights reserved.
Conflict of interest statement
Declaration of interests F.U. has no competing interests. D.Z. reports institutional grants from Genentech, Astra Zeneca, and Plexxikon, as well as personal fees from Genentech, Astra Zeneca, Xencor, Memgen, Takeda, Synthekine, Immunos, and Calidi Biotherapeutics; all of these are outside of the submitted work. D.Z. is an inventor on a patent related to use of oncolytic Newcastle Disease Virus for cancer therapy. F.U. and D.Z. are supported by the National Cancer Institute Cancer Center Core Grant No. P30-CA008748. D.Z. receives additional support from the Ovarian Cancer Research Alliance, GOG Foundation Scholar Investigator Award, and the Department of Defense Ovarian Cancer Research Academy (OC150111).
Comment on
-
Myeloid antigen-presenting cell niches sustain antitumor T cells and license PD-1 blockade via CD28 costimulation.Cancer Cell. 2021 Dec 13;39(12):1623-1642.e20. doi: 10.1016/j.ccell.2021.10.008. Epub 2021 Nov 4. Cancer Cell. 2021. PMID: 34739845 Free PMC article.
Publication types
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources
Medical