{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T20:24:50Z","timestamp":1792787090718,"version":"4.5.0"},"reference-count":70,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2015,9,8]],"date-time":"2015-09-08T00:00:00Z","timestamp":1441670400000},"content-version":"vor","delay-in-days":7,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"BEI Resources Repository"},{"DOI":"10.13039\/100000060","name":"NIAID","doi-asserted-by":"crossref","id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"crossref"}]},{"name":"NIH"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Parasite Immunology"],"published-print":{"date-parts":[[2015,9]]},"abstract":"<jats:title>Summary<\/jats:title>\n                  <jats:p>\n                    Functional impairment of dendritic cells (\n                    <jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content>\n                    s) is part of a survival strategy evolved by\n                    <jats:italic>Leishmania<\/jats:italic>\n                    and\n                    <jats:italic>Plasmodium<\/jats:italic>\n                    parasites to evade host immune responses. Here, the effects of co\u2010exposing human monocyte\u2010derived\n                    <jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content>\n                    s to\n                    <jats:italic>Leishmania\u00a0donovani<\/jats:italic>\n                    promastigotes and\n                    <jats:italic>Plasmodium\u00a0falciparum<\/jats:italic>\n                    \u2010infected erythrocytes were investigated. Co\u2010stimulation resulted in a dual, dose\u2010dependent effect on\n                    <jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content>\n                    differentiation which ranged from semi\u2010mature cells, secreting low interleukin(\u201012p70 levels to a complete lack of phenotypic maturation in the presence of high parasite amounts. The effect was mainly triggered by the\n                    <jats:italic>Leishmania<\/jats:italic>\n                    parasites, as illustrated by their ability to induce semi\u2010mature, interleukin\u201010\u2010producing\n                    <jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content>\n                    s, that poorly responded to lipopolysaccharide stimulation. Conversely,\n                    <jats:italic>P.\u00a0falciparum<\/jats:italic>\n                    blood\u2010stage forms failed to activate\n                    <jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content>\n                    s and only slightly interfered with\n                    <jats:styled-content style=\"fixed-case\">lipopolysaccharide<\/jats:styled-content>\n                    effects. Stimulation with high\n                    <jats:italic>L.\u00a0donovani<\/jats:italic>\n                    concentrations triggered phosphatidylserine translocation, whose onset presented after initiating the maturation impairment process. When added in combination, the two parasites could co\u2010localize in the same\n                    <jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content>\n                    s, confirming that the leading effects of\n                    <jats:italic>Leishmania<\/jats:italic>\n                    over\n                    <jats:italic>Plasmodium<\/jats:italic>\n                    may not be due to mutual exclusion. Altogether, these results suggest that in the presence of visceral leishmaniasis\u2013malaria co\u2010infections,\n                    <jats:italic>Leishmania<\/jats:italic>\n                    \u2010driven effects may overrule the more silent response elicited by\n                    <jats:italic>P.\u00a0falciparum<\/jats:italic>\n                    , shaping host immunity towards a regulatory pattern and possibly delaying disease resolution.\n                  <\/jats:p>","DOI":"10.1111\/pim.12214","type":"journal-article","created":{"date-parts":[[2015,7,14]],"date-time":"2015-07-14T14:50:01Z","timestamp":1436885401000},"page":"453-469","source":"Crossref","is-referenced-by-count":3,"title":["<i>Leishmania donovani<\/i>\n                    infection drives the priming of human monocyte\u2010derived dendritic cells during\n                    <i>Plasmodium falciparum<\/i>\n                    co\u2010infections"],"prefix":"10.1111","volume":"37","author":[{"given":"E.","family":"van den Bogaart","sequence":"first","affiliation":[{"name":"Parasitology Unit Department of Biomedical Research Royal Tropical Institute (KIT) Amsterdam the Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"H. 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R.","family":"Adams","sequence":"additional","affiliation":[{"name":"Parasitology Unit Department of Biomedical Research Royal Tropical Institute (KIT) Amsterdam the Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M. P.","family":"Grobusch","sequence":"additional","affiliation":[{"name":"Division of Internal Medicine Department of Infectious Diseases Center of Tropical Medicine and Travel Medicine Academic Medical Center Amsterdam the Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"I.","family":"van Die","sequence":"additional","affiliation":[{"name":"Department of Molecular Cell Biology VU University Medical Centre (VUMC) Amsterdam the Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"H. D. F. 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