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               <mods:identifier type="citation">Front Immunol. 2016 Nov 4;7:478. eCollection 2016.</mods:identifier>
               <mods:identifier type="doi">10.3389/fimmu.2016.00478</mods:identifier>
               <mods:identifier type="issn">1664-3224</mods:identifier>
               <mods:identifier type="journal">Frontiers in immunology</mods:identifier>
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               <mods:abstract>The complexity of Leishmania-host interactions, one of the main leishmaniasis issues, is yet to be fully understood. We detected elevated IL-27 plasma levels in European patients with active visceral disease caused by Leishmania infantum, which returned to basal levels after successful treatment, suggesting this cytokine as a probable infection mediator. We further addressed this hypothesis recurring to two classical susceptible visceral leishmaniasis mouse models. BALB/c, but not C57BL/6 mice, showed increased IL-27 systemic levels after infection, which was associated with an upregulation of IL-27p28 expression by dendritic cells and higher parasite burdens. Neutralization of IL-27 in acutely infected BALB/c led to decreased parasite burdens and a transient increase in IFN-γ+ splenic T cells, while administration of IL-27 to C57BL/6 promoted a local anti-inflammatory cytokine response at the site of infection and increased parasite loads. Overall, we show that, as in humans, BALB/c IL-27 systemic levels are infection dependently upregulated and may favor parasite installation by controlling inflammation.</mods:abstract>
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                  <mods:topic>IL-27</mods:topic>
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                  <mods:topic>Leishmania infantum</mods:topic>
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                  <mods:title>Interleukin-27 Early Impacts Leishmania infantum Infection in Mice and Correlates with Active Visceral Disease in Humans</mods:title>
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