Open Access
Cell Reports, volume 42, issue 2, pages 112123
XCR1+ DCs are critical for T cell-mediated immunotherapy of chronic viral infections
Domenjo-Vila Eva
1
,
Casella Valentina
1
,
Iwabuchi Ryutaro
2, 3
,
Fossum Even
4
,
Pedragosa Mireia
1
,
Castellvi Quim
5
,
Cebollada Rica Paula
1
,
Kaisho Tsuneyasu
6
,
Terahara Kazutaka
2
,
Bocharov G
7, 8
,
Argilaguet J.
1, 9
,
Meyerhans A
1, 10
1
Infection Biology Laboratory, Department of Medicine and Life Sciences (MELIS), Universitat Pompeu Fabra, Barcelona, Spain
|
2
Department of Immunology, National Institute of Infectious Diseases, Tokyo, Japan
|
3
Department of Life Science and Medical Bioscience, Waseda University, Tokyo, Japan
|
4
5
Department of Information and Communication Technologies, Universitat Pompeu Fabra, Barcelona, Spain
|
6
Department of Immunology, Institute of Advanced Medicine, Wakayama Medical University, Wakayama, Japan
|
10
Institució Catalana de Recerca i Estudis Avançats (iCREA), Barcelona, Spain
|
Publication type: Journal Article
Publication date: 2023-02-15
General Biochemistry, Genetics and Molecular Biology
Abstract
The contribution of cross-presenting XCR1+ dendritic cells (DCs) and SIRPα+ DCs in maintaining T cell function during exhaustion and immunotherapeutic interventions of chronic infections remains poorly characterized. Using the mouse model of chronic LCMV infection, we found that XCR1+ DCs are more resistant to infection and highly activated compared with SIRPα+ DCs. Exploiting XCR1+ DCs via Flt3L-mediated expansion or XCR1-targeted vaccination notably reinvigorates CD8+ T cells and improves virus control. Upon PD-L1 blockade, XCR1+ DCs are not required for the proliferative burst of progenitor exhausted CD8+ T (TPEX) cells but are indispensable to sustain the functionality of exhausted CD8+ T (TEX) cells. Combining anti-PD-L1 therapy with increased frequency of XCR1+ DCs improves functionality of TPEX and TEX subsets, while increase of SIRPα+ DCs dampened their proliferation. Together, this demonstrates that XCR1+ DCs are crucial for the success of checkpoint inhibitor-based therapies through differential activation of exhausted CD8+ T cell subsets.
Citations by journals
1
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Cell Death and Disease
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Cell Death and Disease
1 publication, 100%
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1
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Citations by publishers
1
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Springer Nature
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Springer Nature
1 publication, 100%
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1
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Domenjo-Vila E. et al. XCR1+ DCs are critical for T cell-mediated immunotherapy of chronic viral infections // Cell Reports. 2023. Vol. 42. No. 2. p. 112123.
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Domenjo-Vila E., Casella V., Iwabuchi R., Fossum E., Pedragosa M., Castellvi Q., Cebollada Rica P., Kaisho T., Terahara K., Bocharov G., Argilaguet J., Meyerhans A. XCR1+ DCs are critical for T cell-mediated immunotherapy of chronic viral infections // Cell Reports. 2023. Vol. 42. No. 2. p. 112123.
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TY - JOUR
DO - 10.1016/j.celrep.2023.112123
UR - https://doi.org/10.1016%2Fj.celrep.2023.112123
TI - XCR1+ DCs are critical for T cell-mediated immunotherapy of chronic viral infections
T2 - Cell Reports
AU - Domenjo-Vila, Eva
AU - Casella, Valentina
AU - Iwabuchi, Ryutaro
AU - Fossum, Even
AU - Pedragosa, Mireia
AU - Castellvi, Quim
AU - Cebollada Rica, Paula
AU - Kaisho, Tsuneyasu
AU - Terahara, Kazutaka
AU - Bocharov, G
AU - Argilaguet, J.
AU - Meyerhans, A
PY - 2023
DA - 2023/02/15 00:00:00
PB - Elsevier
SP - 112123
IS - 2
VL - 42
SN - 2211-1247
ER -
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@article{2023_Domenjo-Vila,
author = {Eva Domenjo-Vila and Valentina Casella and Ryutaro Iwabuchi and Even Fossum and Mireia Pedragosa and Quim Castellvi and Paula Cebollada Rica and Tsuneyasu Kaisho and Kazutaka Terahara and G Bocharov and J. Argilaguet and A Meyerhans},
title = {XCR1+ DCs are critical for T cell-mediated immunotherapy of chronic viral infections},
journal = {Cell Reports},
year = {2023},
volume = {42},
publisher = {Elsevier},
month = {feb},
url = {https://doi.org/10.1016%2Fj.celrep.2023.112123},
number = {2},
pages = {112123},
doi = {10.1016/j.celrep.2023.112123}
}
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Domenjo-Vila, Eva, et al. “XCR1+ DCs are critical for T cell-mediated immunotherapy of chronic viral infections.” Cell Reports, vol. 42, no. 2, Feb. 2023, p. 112123. https://doi.org/10.1016%2Fj.celrep.2023.112123.
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