作者: Chieko Shimura , Takahiro Satoh , Ken Igawa , Kosuke Aritake , Yoshihiro Urade
DOI: 10.2353/AJPATH.2010.090111
关键词:
摘要: Prostaglandin D2 (PGD2), an arachidonic acid metabolite, has been implicated in allergic responses. A major source of PGD2 the skin is mast cells that express hematopoietic PGD synthase (H-PGDS). In this study, we show expression H-PGDS human dendritic (DCs) and regulatory mechanisms by which DCs produce PGD2. We detected epidermal Langerhans cells, dermal DCs, plasmacytoid myeloid DCs. Monocyte-derived rapidly secreted when stimulated with calcium ionophore A23187. More importantly, pretreatment monocyte-derived PMA (phorbol 12-myrisate 13-acetate) synergistically enhanced rapid secretion induced A23187, whereas alone did not induce secretion. Lipopolysaccharide (LPS) reduced expression, but interferon-γ followed LPS significant production a delayed time course at 6 hours. This effect was associated inhibition LPS-induced reduction. Interestingly, irritant compound, SDS, also release. CCL22/macrophage-derived chemokine synthesis interferon-γ-treated keratinocytes. addition, bone marrow-derived from wild-type mice lymph node to higher amounts interleukin-17 than lacking gene. Thus, could be important may mediate or regulate inflammation releasing response various stimuli, contributing innate and/or acquired immune