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               <mods:identifier type="citation">Aging (Albany NY)  . 2023;15(6):1791-1807.</mods:identifier>
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               <mods:identifier type="doi">10.18632/aging.204598</mods:identifier>
               <mods:identifier type="e-issn">1945-4589</mods:identifier>
               <mods:identifier type="journal">Aging</mods:identifier>
               <mods:abstract>Antibodies targeting the PD-1 receptor and its ligand PD-L1 have shown impressive responses in some tumors of bad prognosis. We hypothesized that, since immunosuppressive cells might present several immune checkpoints on their surface, the selective elimination of PD-L1 expressing cells could be efficacious in enabling the activation of antitumoral immune responses. To address this question, we developed an inducible suicidal knock-in mouse allele of Pd-l1 (PD-L1ATTAC) which allows for the tracking and specific elimination of PD-L1-expressing cells in adult tissues. Consistent with our hypothesis, elimination of PD-L1 expressing cells from the mouse peritoneum increased the septic response to lipopolysaccharide (LPS), due to an exacerbated inflammatory response to the endotoxin. In addition, mice depleted of PD-L1+ cells were resistant to colon cancer peritoneal allografts, which was associated with a loss of immunosuppressive B cells and macrophages, concomitant with an increase in activated cytotoxic CD8 T cells. Collectively, these results illustrate the usefulness of PD-L1ATTAC mice for research in immunotherapy and provide genetic support to the concept of targeting PD-L1 expressing cells in cancer.</mods:abstract>
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                  <mods:title>PD-L1ATTAC mice reveal the potential of depleting PD-L1 expressing cells in cancer therapy.</mods:title>
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