XCR1+ DCs are critical for T cell-mediated immunotherapy of chronic viral infections

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 r...

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Published inCell reports (Cambridge) Vol. 42; no. 2; p. 112123
Main Authors Domenjo-Vila, Eva, Casella, Valentina, Iwabuchi, Ryutaro, Fossum, Even, Pedragosa, Mireia, Castellví, Quim, Cebollada Rica, Paula, Kaisho, Tsuneyasu, Terahara, Kazutaka, Bocharov, Gennady, Argilaguet, Jordi, Meyerhans, Andreas
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 28.02.2023
Elsevier
Subjects
anti-PD-L1
chronic infection
CP: Immunology
Flt3L
immunotherapy
LCMV
SIRPɑ+ DCs
T cell exhaustion
therapeutic vaccination
XCR1+ DCs
anti-PD-L1
CP: Immunology
LCMV
chronic infection
therapeutic vaccination
immunotherapy
T cell exhaustion
Flt3L
XCR1+ DCs
SIRPɑ+ DCs
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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. [Display omitted] •XCR1+ DCs are more functional and less prone to LCMV infection than SIRPα+ DCs•Expanding XCR1+ DCs via Flt3L or delivering XCR1-targeting Ag improve virus control•Anti-PD-L1 treatment increases XCR1+ DC numbers and IL-12 production•XCR1+ DCs promote TEX functionality but are dispensable for TPEX proliferation burst Domenjo-Vila et al. show that XCR1+ DCs are crucial in augmenting exhausted CD8+ T cell effector functions during immunotherapeutic interventions in chronic virus infections. Increased T cell functionality leads to reduced virus loads. XCR1+ DCs should be among the preferential targets in immunotherapeutic cure strategies.
AbstractList 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.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.
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.
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 (T ) cells but are indispensable to sustain the functionality of exhausted CD8+ T (T ) cells. Combining anti-PD-L1 therapy with increased frequency of XCR1+ DCs improves functionality of T and T 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.
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. [Display omitted] •XCR1+ DCs are more functional and less prone to LCMV infection than SIRPα+ DCs•Expanding XCR1+ DCs via Flt3L or delivering XCR1-targeting Ag improve virus control•Anti-PD-L1 treatment increases XCR1+ DC numbers and IL-12 production•XCR1+ DCs promote TEX functionality but are dispensable for TPEX proliferation burst Domenjo-Vila et al. show that XCR1+ DCs are crucial in augmenting exhausted CD8+ T cell effector functions during immunotherapeutic interventions in chronic virus infections. Increased T cell functionality leads to reduced virus loads. XCR1+ DCs should be among the preferential targets in immunotherapeutic cure strategies.
ArticleNumber 112123
Author Domenjo-Vila, Eva
Pedragosa, Mireia
Cebollada Rica, Paula
Kaisho, Tsuneyasu
Argilaguet, Jordi
Terahara, Kazutaka
Casella, Valentina
Iwabuchi, Ryutaro
Bocharov, Gennady
Fossum, Even
Castellví, Quim
Meyerhans, Andreas
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Issue 2
Keywords anti-PD-L1
CP: Immunology
LCMV
chronic infection
therapeutic vaccination
immunotherapy
T cell exhaustion
Flt3L
XCR1+ DCs
SIRPɑ+ DCs
Language English
License This is an open access article under the CC BY license.
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Snippet The contribution of cross-presenting XCR1+ dendritic cells (DCs) and SIRPα+ DCs in maintaining T cell function during exhaustion and immunotherapeutic...
The contribution of cross-presenting XCR1+ dendritic cells (DCs) and SIRPα+ DCs in maintaining T cell function during exhaustion and immunotherapeutic...
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SubjectTerms anti-PD-L1
chronic infection
CP: Immunology
Flt3L
immunotherapy
LCMV
SIRPɑ+ DCs
T cell exhaustion
therapeutic vaccination
XCR1+ DCs
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Title XCR1+ DCs are critical for T cell-mediated immunotherapy of chronic viral infections
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