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RISS 인기검색어
- 검색키워드
- 저자 : Mayumi Saeki (검색결과 3 건)
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Mechanism of Macrophage-Derived Chemokine/CCL22 Production by HaCaT Keratinocytes
( Chizuko Yano ),( Hidehisa Saeki ),( Mayumi Komine ),( Shinji Kagami ),( Yuichiro Tsunemi ),( Mamitaro Ohtsuki ),( Hidemi Nakagawa ) 대한피부과학회 2015 Annals of Dermatology Vol.27 No.2
Background: CC chemokine ligand 17 (CCL17) and CCL22 are the functional ligands for CCR4. We previously reported that inhibitors of nuclear factor-kappa B and p38 mitogen- activated protein kinase (p38 MAPK), but not of extracellular signal-related kinase (ERK), inhibited tumor necrosis factor (TNF)-α- and interferon (IFN)-γ-induced production of CCL17 by the human keratinocyte cell line, HaCaT. Further, an inhibitor of epidermal growth factor receptor (EGFR) enhanced the CCL17 production by these keratinocytes. Objective: To identify the mechanism underlying CCL22 production by HaCaT cells. Methods: We investigated the signal transduction pathways by which TNF-α and IFN-γ stimulate HaCaT cells to produce CCL22 by adding various inhibitors. Results: TNF-α- and IFN-γ- induced CCL22 production was inhibited by PD98059, PD153035, Bay 11-7085, SB202190, c-Jun N-terminal kinase (JNK) inhibitor II, and Janus kinase (JAK) inhibitor 1. Conclusion: Our results indicate that CCL22 production in HaCaT cells is dependent on ERK, EGFR, p38 MAPK, JNK, and JAK and is mediated by different signal pathways from those regulating CCL17 production. Altogether, our previous and present results suggest that EGFR activation represses CCL17 but enhances CCL22 production by these cells.(Ann Dermatol 27(2) 152∼156, 2015)
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Mechanism of Macrophage-Derived Chemokine/CCL22 Production by HaCaT Keratinocytes
( Chizuko Yano ),( Hidehisa Saeki ),( Mayumi Komine ),( Shinji Kagami ),( Yuichiro Tsunemi ),( Mamitaro Ohtsuki ),( Hidemi Nakagawa ) 대한피부과학회 2015 Annals of Dermatology Vol.27 No.3
Background: CC chemokine ligand 17 (CCL17) and CCL22 are the functional ligands for CCR4. We previously reported that inhibitors of nuclear factor-kappa B and p38 mitogen- activated protein kinase (p38 MAPK), but not of extracellular signal-related kinase (ERK), inhibited tumor necrosis factor (TNF)-α- and interferon (IFN)-γ-induced production of CCL17 by the human keratinocyte cell line, HaCaT. Further, an inhibitor of epidermal growth factor receptor (EGFR) enhanced the CCL17 production by these keratinocytes. Objective: To identify the mechanism underlying CCL22 production by HaCaT cells. Methods: We investigated the signal transduction pathways by which TNF-α and IFN-γ stimulate HaCaT cells to produce CCL22 by adding various inhibitors. Results: TNF-α- and IFN-γ- induced CCL22 production was inhibited by PD98059, PD153035, Bay 11-7085, SB202190, c-Jun N-terminal kinase (JNK) inhibitor II, and Janus kinase (JAK) inhibitor 1. Conclusion: Our results indicate that CCL22 production in HaCaT cells is dependent on ERK, EGFR, p38 MAPK, JNK, and JAK and is mediated by different signal pathways from those regulating CCL17 production. Altogether, our previous and present results suggest that EGFR activation represses CCL17 but enhances CCL22 production by these cells. (Ann Dermatol 27(2) 152∼156, 2015)
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T-Helper Type 2 Cells Direct Antigen-Induced Eosinophilic Skin Inflammation in Mice
Osamu Kaminuma,Tomoe Nishimura,Noriko Kitamura,Mayumi Saeki,Takachika Hiroi,Akio Mori 대한천식알레르기학회 2018 Allergy, Asthma & Immunology Research Vol.10 No.1
Eosinophilic inflammation in combination with immunoglobulin E (IgE) production is a characteristic feature of atopic dermatitis. Although activated T-helper type (Th) 2 cells play critical roles in the local accumulation and activation of eosinophils, whether they induce eosinophilic skin inflammation, independent of the IgE-mediated pathway has been unclear. To address the functional role of T cells in allergic skin diseases, we herein transferred Th1/Th2-differentiated or naive DO11.10 T cells into unprimed BALB/c mice. Ovalbumin-specific Th2 cells, as well as eosinophils, accumulated in the skin upon antigen challenge, despite the absence of antigen-specific IgE. Neither antigen-specific Th1 nor naive T cells induced eosinophil accumulation, although Th1 cells by themselves migrated into the skin. Interleukin (IL)-4, IL-5, and eotaxin were specifically produced in the skin of antigen-challenged, Th2 cell-transferred mice, whereas interferon (IFN)-γ and regulated on activation, normal T cell expressed and secreted (RANTES) were preferentially produced in Th1 cells-transferred mice. Production of monocyte chemoattractant protein (MCP)-1 and MCP-3 was enhanced by both Th1 and Th2 cells. The accumulation of eosinophils and Th2 cells in the skin was suppressed by both dexamethasone and FK506, indicating an essential role of Th2 cells in eosinophil recruitment. We conclude that Th2 cells can induce eosinophilic infiltration into the skin in the absence of antigen-specific IgE.
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