Distinct MAPK pathways are involved in IL-23 production in dendritic cells cocultured with NK cells in the absence or presence of angiotensin II

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• 作者：Lin Yang^a ; Changqing Du^b ; Ting Chen^a ; Shan Li^a ; Wencheng Nie^a ; Weiguo Zhu^a ; Fangyan Fan^a ; Jianhua Zhu^a ; ^{jhzhu2006@hotmail.com} ; Hui Yan^a ; ^{Michelle2000@126.com}
• 关键词：DCs ; dendritic cells ; NK ; natural killer ; TNF-邪 ; tumor necrosis factor-伪 ; IL-12 ; interleukin-12 ; IFN-纬 ; interferon-纬 ; APC ; activated antigen-presenting cells ; Ang II ; angiotensin II ; RAS ; the major bioactive peptide of the renin&ndash ; angiotensin syst
• 刊名：Molecular Immunology
• 出版年：2012
• 期刊代码：112_01615890
• 类别：bio
• 出版时间：May, 2012
• 卷：51
• 期：1
• 页码：51-56
• 文件大小：586 K

摘要

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.