title: Distinct MAPK pathways are involved in IL-23 production in dendritic cells cocultured with NK cells in the absence or presence of angiotensin II.
abstract: Accumulated evidence suggests that the crosstalk between dendritic cells (DCs) and natural killer (NK) cells enhances each other's capacity, and results in the production of a variety of soluble factors. However, little is known about the effect of DC-NK crosstalk in interleukin-23 (IL-23) production. In the present study we show that DC-NK coculture caused a high expression of IL-23, angiotensin II (Ang II) alone moderately increased IL-23 production in DCs, but decreased IL-23 secretion in the DC-NK coculture system. We found that Ang II does not influence DC maturation in DC-NK crosstalk. We next investigated the mitogen-activated protein kinase (MAPK) pathway in DCs. We found that Ang II increased IL-23 production through the extracellular signal-related kinase (ERK) pathway. All three MAPK members c-Jun N-terminal kinase (JNK), ERK and p38 were involved in IL-23 production in the DC-NK coculture system. In the presence of Ang II, only the JNK pathway seems to play a role in IL-23 production in DCs cocultured with NK. These data suggest that distinct MAPK pathways are involved in IL-23 production in DCs in response to different stimuli. This work demonstrates for the first time that IL-23 is produced in the DC-NK coculture system, and that Ang II is involved in DC-NK crosstalk. This data will act as a resource that allows further exploitation of role of immune response in atherosclerosis.
authors.affiliation: Department of Cardiology, First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, PR China.
authors.forename: Lin
authors.initials: L
authors.lastname: Yang
authors.forename: Changqing
authors.initials: C
authors.lastname: Du
authors.forename: Ting
authors.initials: T
authors.lastname: Chen
authors.forename: Shan
authors.initials: S
authors.lastname: Li
authors.forename: Wencheng
authors.initials: W
authors.lastname: Nie
authors.forename: Weiguo
authors.initials: W
authors.lastname: Zhu
authors.forename: Fangyan
authors.initials: F
authors.lastname: Fan
authors.forename: Jianhua
authors.initials: J
authors.lastname: Zhu
authors.forename: Hui
authors.initials: H
authors.lastname: Yan
mesh_terms: D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D050197:Atherosclerosis / Q000276:immunology / Q000378:metabolism; D001854:Bone Marrow Cells / Q000378:metabolism; D002450:Cell Communication; D002478:Cells, Cultured; D018920:Coculture Techniques; D003713:Dendritic Cells / Q000378:metabolism*; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism; D005260:Female; D053759:Interleukin-23 / Q000096:biosynthesis*; D048031:JNK Mitogen-Activated Protein Kinases / Q000378:metabolism; D007694:Killer Cells, Natural / Q000502:physiology*; D020935:MAP Kinase Signaling System; D051379:Mice; D008810:Mice, Inbred C57BL; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism
chemical_list: D053759:Interleukin-23; D000804:Angiotensin II; D048049:Extracellular Signal-Regulated MAP Kinases; D048031:JNK Mitogen-Activated Protein Kinases; D048051:p38 Mitogen-Activated Protein Kinases