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Using a prototypic model of intracellular infection, we previously showed that<jats:italic>Leishmania major<\/jats:italic>parasites prime human DC for efficient interleukin-12 (IL-12) secretion.<jats:italic>L. major<\/jats:italic>infection is associated with self-limiting cutaneous disease and powerful immunity. In stark contrast, the causative agent of visceral leishmaniasis,<jats:italic>Leishmania donovani<\/jats:italic>, does not prime human DC for IL-12 production. Here, we report that DC priming by<jats:italic>L. major<\/jats:italic>infection results in the early activation of NF-\u03baB transcription factors and the up-regulation and nuclear translocation of interferon regulatory factor 1 (IRF-1) and IRF-8. The inhibition of NF-\u03baB activation by the pretreatment of DC with caffeic acid phenethyl ester blocks<jats:italic>L. major<\/jats:italic>-induced IRF-1 and IRF-8 activation and IL-12 expression. We further demonstrate that IRF-1 and IRF-8 obtained from<jats:italic>L. major<\/jats:italic>-infected human DC specifically bind to their consensus binding sites on the<jats:italic>IL-12p35<\/jats:italic>promoter, indicating that<jats:italic>L. major<\/jats:italic>infection either directly stimulates a signaling cascade or induces an autocrine pathway that activates IRF-1 and IRF-8, ultimately resulting in<jats:italic>IL-12<\/jats:italic>transcription.<\/jats:p>","DOI":"10.1128\/iai.01252-07","type":"journal-article","created":{"date-parts":[[2008,3,4]],"date-time":"2008-03-04T01:35:04Z","timestamp":1204594504000},"page":"2138-2148","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":41,"title":["<i>Leishmania major<\/i>Infection Activates NF-\u03baB and Interferon Regulatory Factors 1 and 8 in Human Dendritic Cells"],"prefix":"10.1128","volume":"76","author":[{"given":"Asha","family":"Jayakumar","sequence":"first","affiliation":[{"name":"Center for Global Health and Infectious Diseases, Department of Biological Sciences, University of Notre Dame, Notre Dame, Indiana 46556"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael J.","family":"Donovan","sequence":"additional","affiliation":[{"name":"Center for Global Health and Infectious Diseases, Department of Biological Sciences, University of Notre Dame, Notre Dame, Indiana 46556"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vinita","family":"Tripathi","sequence":"additional","affiliation":[{"name":"Center for Global Health and Infectious Diseases, Department of Biological Sciences, University of Notre Dame, Notre Dame, Indiana 46556"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marcelo","family":"Ramalho-Ortigao","sequence":"additional","affiliation":[{"name":"Center for Global Health and Infectious Diseases, Department of Biological Sciences, University of Notre Dame, Notre Dame, Indiana 46556"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mary Ann","family":"McDowell","sequence":"additional","affiliation":[{"name":"Center for Global Health and Infectious Diseases, Department of Biological Sciences, University of Notre Dame, Notre Dame, Indiana 46556"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0706421"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.162.1.324"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0008-8749(03)00114-X"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2002-10-3232"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.172.2.1186"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.97.1.91"},{"key":"e_1_3_2_8_2","doi-asserted-by":"crossref","first-page":"617","DOI":"10.4049\/jimmunol.143.2.617","volume":"143","year":"1989","unstructured":"Da Silva, R. 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