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Myeloid antigen-presenting cells (APCs) are most likely involved in the induction and expression of the underlying inflammatory responses. To study the interaction of human APC subsets with<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">H. pylori<\/jats:named-content>, we infected monocytes, monocyte-derived dendritic cells (DCs), and monocyte-derived (classically activated; M1) macrophages with<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">H. pylori<\/jats:named-content>and analyzed phenotypic alterations, cytokine secretion, phagocytosis, and immunostimulation. Since we detected CD163<jats:sup>+<\/jats:sup>(alternatively activated; M2) macrophages in gastric biopsy specimens from<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">H. pylori<\/jats:named-content>-positive patients, we also included monocyte-derived M2 macrophages in the study. Upon<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">H. pylori<\/jats:named-content>infection, monocytes secreted interleukin-1\u03b2 (IL-1\u03b2), IL-6, IL-10, and IL-12p40 (partially secreted as IL-23) but not IL-12p70. Infected DCs became activated, as shown by the enhanced expression of CD25, CD80, CD83, PDL-1, and CCR7, and secreted IL-1\u03b2, IL-6, IL-10, IL-12p40, IL-12p70, and IL-23. However, infection led to significantly downregulated CD209 and suppressed the constitutive secretion of macrophage migration inhibitory factor (MIF).<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">H. pylori<\/jats:named-content>-infected M1 macrophages upregulated CD14 and CD32, downregulated CD11b and HLA-DR, and secreted mainly IL-1\u03b2, IL-6, IL-10, IL-12p40, and IL-23. Activation of DCs and M1 macrophages correlated with increased capacity to induce T-cell proliferation and decreased phagocytosis of dextran. M2 macrophages upregulated CD14 and CD206 and secreted IL-10 but produced less of the proinflammatory cytokines than M1 macrophages. Thus,<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">H. pylori<\/jats:named-content>affects the functions of human APC subsets differently, which may influence the course and the outcome of<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">H. pylori<\/jats:named-content>infection. The suppression of MIF in DCs constitutes a novel immune evasion mechanism exploited by<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">H. pylori<\/jats:named-content>.<\/jats:p>","DOI":"10.1128\/iai.00381-12","type":"journal-article","created":{"date-parts":[[2012,5,22]],"date-time":"2012-05-22T02:54:20Z","timestamp":1337655260000},"page":"2724-2734","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":86,"title":["Comparative Analysis of the Interaction of Helicobacter pylori with Human Dendritic Cells, Macrophages, and Monocytes"],"prefix":"10.1128","volume":"80","author":[{"given":"Michael","family":"Fehlings","sequence":"first","affiliation":[{"name":"Institute of Tropical Medicine and International Health, Charit\u00e9-Universit\u00e4tsmedizin Berlin, Berlin, Germany"},{"name":"Department of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lea","family":"Drobbe","sequence":"additional","affiliation":[{"name":"Department of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Verena","family":"Moos","sequence":"additional","affiliation":[{"name":"Medical Clinic I, Charit\u00e9-Universit\u00e4tsmedizin Berlin, Berlin, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pablo","family":"Renner Viveros","sequence":"additional","affiliation":[{"name":"Institute of Tropical Medicine and International Health, Charit\u00e9-Universit\u00e4tsmedizin Berlin, Berlin, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jana","family":"Hagen","sequence":"additional","affiliation":[{"name":"Institute of Tropical Medicine and International Health, Charit\u00e9-Universit\u00e4tsmedizin Berlin, Berlin, Germany"},{"name":"Department of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Macarena","family":"Beigier-Bompadre","sequence":"additional","affiliation":[{"name":"Department of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ervinna","family":"Pang","sequence":"additional","affiliation":[{"name":"Department of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elena","family":"Belogolova","sequence":"additional","affiliation":[{"name":"Department of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuri","family":"Churin","sequence":"additional","affiliation":[{"name":"Department of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas","family":"Schneider","sequence":"additional","affiliation":[{"name":"Medical Clinic I, Charit\u00e9-Universit\u00e4tsmedizin Berlin, Berlin, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas F.","family":"Meyer","sequence":"additional","affiliation":[{"name":"Department of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Toni","family":"Aebischer","sequence":"additional","affiliation":[{"name":"Department of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany"},{"name":"Robert Koch Institute, Berlin, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ralf","family":"Ignatius","sequence":"additional","affiliation":[{"name":"Institute of Tropical Medicine and International Health, Charit\u00e9-Universit\u00e4tsmedizin Berlin, Berlin, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1038\/ni1496"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.3109\/08923970902947317"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI27177"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0966-842X(00)01875-8"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.170.4.1635"},{"key":"e_1_3_3_7_2","first-page":"2939","article-title":"Helicobacter pylori eradication shifts monocyte Fc\u03b3 receptor balance toward inhibitory Fc\u03b3RIIB in immune thrombocytopenic purpura patients","volume":"118","author":"Asahi A","year":"2008","unstructured":"AsahiA. 2008. 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