title: IL-27 improves migrational and antiviral potential of CB dendritic cells.
abstract: Interleukin (IL)-27 is known to be increased considerably in cord blood (CB) dendritic cells (DCs) after TLR ligation. Previously, we demonstrated that also basal IL-27 levels are higher in CB DCs. Here, we examined effects of IL-27 on monocyte derived dendritic cells (moDCs) to approach its particular role in the specialized immune system of the human neonate. Exogenous IL-27 promotes IL-27 transcription in CB and adult blood (AB) moDCs. IL-27 acts on CB moDCs primarily by significantly augmenting IL-27 protein, secondarily by increasing transcription of CXCL10 among other chemokines, chemokine receptor CCR1, interferon stimulated genes, transcription factor IRF8 and genes involved in antigen presentation. Furthermore, CB moDCs respond to IL-27 with augmented IL-8 and Tumor necrosis factor (TNF)-α. The results suggest that IL-27 enhances migrational and antiviral properties of CB dendritic cells.
authors: Pediatric Immunology Mainz, Children's Hospital, Medical Center of the Johannes Gutenberg University Mainz, Germany. Electronic address: juliatar@students.uni-mainz.de.
authors: Julia
authors: J
authors: Birkholz
authors: Pediatric Immunology Mainz, Children's Hospital, Medical Center of the Johannes Gutenberg University Mainz, Germany.
authors: Aysefa
authors: A
authors: Doganci
authors: Pediatric Immunology Mainz, Children's Hospital, Medical Center of the Johannes Gutenberg University Mainz, Germany.
authors: Claudia
authors: C
authors: Darstein
authors: Pediatric Immunology Mainz, Children's Hospital, Medical Center of the Johannes Gutenberg University Mainz, Germany.
authors: Stephan
authors: S
authors: Gehring
authors: Pediatric Immunology Mainz, Children's Hospital, Medical Center of the Johannes Gutenberg University Mainz, Germany.
authors: Fred
authors: F
authors: Zepp
authors: Pediatric Immunology Mainz, Children's Hospital, Medical Center of the Johannes Gutenberg University Mainz, Germany.
authors: Claudius U
authors: CU
authors: Meyer
mesh_terms: D000328:Adult; D002454:Cell Differentiation; D002465:Cell Movement / Q000187:drug effects*; D002478:Cells, Cultured; D054357:Chemokine CXCL10 / Q000235:genetics / Q000378:metabolism; D003713:Dendritic Cells / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D005312:Fetal Blood / Q000166:cytology* / Q000378:metabolism; D005786:Gene Expression Regulation; D006801:Humans; D007231:Infant, Newborn; D050835:Interferon Regulatory Factors / Q000235:genetics / Q000378:metabolism; D016209:Interleukin-8 / Q000235:genetics / Q000378:metabolism; D007378:Interleukins / Q000096:biosynthesis / Q000235:genetics* / Q000494:pharmacology; D009000:Monocytes / Q000166:cytology / Q000378:metabolism; D054389:Receptors, CCR1 / Q000235:genetics / Q000378:metabolism; D050794:STAT1 Transcription Factor / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction; D014158:Transcription, Genetic; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism; D000099185:Interferon Regulatory Factor-8
chemical_list: D054357:Chemokine CXCL10; D050835:Interferon Regulatory Factors; D016209:Interleukin-8; D007378:Interleukins; D054389:Receptors, CCR1; D050794:STAT1 Transcription Factor; D014409:Tumor Necrosis Factor-alpha; D000099185:Interferon Regulatory Factor-8; C515300:CCR1 protein, human; C114753:CXCL10 protein, human; C464565:MYDGF protein, human; C494079:STAT1 protein, human