Progenitor exhausted PD-1+ T cells are cellular targets of immune checkpoint inhibition in atherosclerosis
(2025) In Nature Cardiovascular Research 4(10). p.1311-1328- Abstract
Immune checkpoint inhibitors (ICIs), targeting checkpoint receptors such as programmed cell death protein 1 (PD-1), are associated with increased risk of cardiovascular events, but the underlying mechanisms remain poorly understood. Here we show that PD-1 + T cells from murine atherosclerotic aortas mainly display a progenitor exhausted phenotype (PD-1 intSlamf6 +Tim3 -), produce IFNγ in vivo, exhibit signs of recent proliferation and maintain polyfunctionality. PD-1 blockade induced marked changes in plaque immune phenotype, with increased PD-1 high T cell accumulation, IFNγ production, formation of lymphocyte foci and neutrophil recruitment. Depletion of PD-1 high T cells prior to PD-1 blockade did not impede T cell recruitment,... (More)
Immune checkpoint inhibitors (ICIs), targeting checkpoint receptors such as programmed cell death protein 1 (PD-1), are associated with increased risk of cardiovascular events, but the underlying mechanisms remain poorly understood. Here we show that PD-1 + T cells from murine atherosclerotic aortas mainly display a progenitor exhausted phenotype (PD-1 intSlamf6 +Tim3 -), produce IFNγ in vivo, exhibit signs of recent proliferation and maintain polyfunctionality. PD-1 blockade induced marked changes in plaque immune phenotype, with increased PD-1 high T cell accumulation, IFNγ production, formation of lymphocyte foci and neutrophil recruitment. Depletion of PD-1 high T cells prior to PD-1 blockade did not impede T cell recruitment, suggesting a role for progenitor exhausted PD-1 int T cells in ICI-driven T cell plaque accumulation. Human circulating PD-1 + T cells produced IFNγ and were associated with subclinical coronary atherosclerosis. Our studies highlight IFNγ-producing PD-1 + T cells as a potential key immune cell population mediating increased cardiovascular risk in patients with cancer receiving ICI.
(Less)
- author
- organization
-
- Cardiovascular research - Immune regulation (research group)
- EXODIAB: Excellence of Diabetes Research in Sweden
- Cardiovascular Research - Immunity and Atherosclerosis (research group)
- Cardiovascular Research - Cellular Metabolism and Inflammation (research group)
- Synthetic Immunology (research group)
- Cardiac Inflammation Research Group (research group)
- Diabetic Complications (research group)
- EpiHealth: Epidemiology for Health
- Teachers at the Medical Programme
- Cardiovascular Research - Matrix and Inflammation in Atherosclerosis (research group)
- publishing date
- 2025-10-07
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Nature Cardiovascular Research
- volume
- 4
- issue
- 10
- pages
- 1311 - 1328
- publisher
- Nature Publishing Group
- external identifiers
-
- scopus:105018846142
- pmid:41057609
- ISSN
- 2731-0590
- DOI
- 10.1038/s44161-025-00713-2
- language
- English
- LU publication?
- yes
- additional info
- © 2025. The Author(s).
- id
- 02df2a4d-7b28-4209-80f4-9c184546a922
- date added to LUP
- 2025-10-13 09:08:58
- date last changed
- 2025-12-19 16:20:06
@article{02df2a4d-7b28-4209-80f4-9c184546a922,
abstract = {{<p>Immune checkpoint inhibitors (ICIs), targeting checkpoint receptors such as programmed cell death protein 1 (PD-1), are associated with increased risk of cardiovascular events, but the underlying mechanisms remain poorly understood. Here we show that PD-1 + T cells from murine atherosclerotic aortas mainly display a progenitor exhausted phenotype (PD-1 intSlamf6 +Tim3 -), produce IFNγ in vivo, exhibit signs of recent proliferation and maintain polyfunctionality. PD-1 blockade induced marked changes in plaque immune phenotype, with increased PD-1 high T cell accumulation, IFNγ production, formation of lymphocyte foci and neutrophil recruitment. Depletion of PD-1 high T cells prior to PD-1 blockade did not impede T cell recruitment, suggesting a role for progenitor exhausted PD-1 int T cells in ICI-driven T cell plaque accumulation. Human circulating PD-1 + T cells produced IFNγ and were associated with subclinical coronary atherosclerosis. Our studies highlight IFNγ-producing PD-1 + T cells as a potential key immune cell population mediating increased cardiovascular risk in patients with cancer receiving ICI. </p>}},
author = {{Mulholland, Megan and Chalou, Anthi and Andersson, Samuel H A and Depuydt, Marie A C and Yu, Yinda and Lin, Shiying and Tallbäck, Klara and Ericsson, Astrid and Jakobsson, Gabriel and de Mol, Jill and Kryvokhyzha, Dmytro and Lichtman, Andrew H and Foks, Amanda C and Schiopu, Alexandru and Björkbacka, Harry and Slütter, Bram and Gisterå, Anton and Engelbertsen, Daniel}},
issn = {{2731-0590}},
language = {{eng}},
month = {{10}},
number = {{10}},
pages = {{1311--1328}},
publisher = {{Nature Publishing Group}},
series = {{Nature Cardiovascular Research}},
title = {{Progenitor exhausted PD-1<sup>+</sup> T cells are cellular targets of immune checkpoint inhibition in atherosclerosis}},
url = {{http://dx.doi.org/10.1038/s44161-025-00713-2}},
doi = {{10.1038/s44161-025-00713-2}},
volume = {{4}},
year = {{2025}},
}
