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oai:repisalud.isciii.es:20.500.12105/89602025-06-09T09:39:15Zcom_20.500.12105_2052com_20.500.12105_2051col_20.500.12105_19609

00925njm 22002777a 4500 dc Pérez-Cabezas, Begoña author Cecílio, Pedro author Robalo, Ana Luisa author Silvestre, Ricardo author Carrillo, Eugenia author Moreno, Javier author San Martín, Juan Víctor author Vasconcellos, Rita author Cordeiro-da-Silva, Anabela author 2016 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. Front Immunol. 2016 Nov 4;7:478. eCollection 2016. 10.3389/fimmu.2016.00478 1664-3224 Frontiers in immunology 27867384 http://hdl.handle.net/20.500.12105/8960 IL-27 Leishmania infantum Human Immune regulation Mouse models Interleukin-27 Early Impacts Leishmania infantum Infection in Mice and Correlates with Active Visceral Disease in Humans