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                  <mods:namePart>Casella, Valentina</mods:namePart>
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                  <mods:namePart>Domenjo-Vila, Eva</mods:namePart>
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                  <mods:namePart>Esteve-Codina, Anna</mods:namePart>
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                  <mods:namePart>Pedragosa, Mireia</mods:namePart>
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                  <mods:namePart>Cebollada Rica, Paula</mods:namePart>
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                  <mods:namePart>Vidal, Enric</mods:namePart>
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                  <mods:namePart>de la Rubia, Ivan</mods:namePart>
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                  <mods:namePart>López-Rodríguez, Cristina</mods:namePart>
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                  <mods:namePart>Argilaguet, Jordi</mods:namePart>
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                  <mods:namePart>Meyerhans, Andreas</mods:namePart>
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                  <mods:namePart>Producció Animal</mods:namePart>
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                  <mods:dateAccessioned encoding="iso8601">2025-10-22T11:24:14Z</mods:dateAccessioned>
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                  <mods:dateIssued encoding="iso8601">2023-12-18</mods:dateIssued>
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               <mods:identifier type="citation">Casella, Valentina, Eva Domenjo-Vila, Anna Esteve‐Codina, Mireia Pedragosa, Paula Cebollada Rica, Enríc Vidal, Ivan De La Rubia, et al. 2023. “Differential Kinetics of Splenic CD169+ Macrophage Death Is One Underlying Cause of Virus Infection Fate Regulation.” Cell Death and Disease 14 (12): 838. doi:10.1038/s41419-023-06374-y.</mods:identifier>
               <mods:identifier type="issn">2041-4889</mods:identifier>
               <mods:identifier type="uri">http://hdl.handle.net/20.500.12327/2855</mods:identifier>
               <mods:identifier type="doi">https://doi.org/10.1038/s41419-023-06374-y</mods:identifier>
               <mods:abstract>Acute infection and chronic infection are the two most common fates of pathogenic virus infections. While several factors that&#xd;
contribute to these fates are described, the critical control points and the mechanisms that underlie infection fate regulation are&#xd;
incompletely understood. Using the acute and chronic lymphocytic choriomeningitis virus (LCMV) infection model of mice, we find&#xd;
that the early dynamic pattern of the IFN-I response is a differentiating trait between both infection fates. Acute-infected mice&#xd;
generate a 2-wave IFN-I response while chronic-infected mice generate only a 1-wave response. The underlying cause is a temporal&#xd;
difference in CD8 T cell-mediated killing of splenic marginal zone CD169+ macrophages. It occurs later in acute infection and thus&#xd;
enables CD169+ marginal zone macrophages to produce the 2nd IFN-I wave. This is required for subsequent immune events&#xd;
including induction of inflammatory macrophages, generation of effector CD8+ T cells and virus clearance. Importantly, these&#xd;
benefits come at a cost for the host in the form of spleen fibrosis. Due to an earlier marginal zone destruction, these ordered&#xd;
immune events are deregulated in chronic infection. Our findings demonstrate the critical importance of kinetically wellcoordinated sequential immune events for acute infection control and highlights that it may come at a cost for the host organism.</mods:abstract>
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                  <mods:title>Differential kinetics of splenic CD169+ macrophage death is one underlying cause of virus infection fate regulation</mods:title>
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