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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)
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)
Suppressive Effects of Mesenchymal Stem Cells in Adipose Tissue on Allergic Contact Dermatitis
( Sota Kikuchi ),( Koichi Yanaba ),( Yoshimasa Nobeyama ),( Shigeharu Yabe ),( Masahiro Kiso ),( Hidehisa Saeki ),( Yayoi Tada ),( Hidemi Nakagawa ),( Hitoshi Okochi ) 대한피부과학회 2017 Annals of Dermatology Vol.29 No.4
Background: Allergic contact dermatitis (ACD), which is ac-celerated by interferon (IFN)-γ and suppressed by inter-leukin (IL)-10 as regulators, is generally self-limited after re-moval of the contact allergen. Adipose tissue-derived multi-potent mesenchymal stem cells (ASCs) potentially exert im-munomodulatory effects. Considering that subcutaneous adipose tissue is located close to the site of ACD and includes mesenchymal stem cells (MSCs), the MSCs in adipose tissue could contribute to the self-limiting course of ACD. Objective: The aims of the present study were to elucidate the effects of MSCs in adipose tissue on ACD and to examine any cyto-kine- mediated mechanisms involved. Methods: Ear thick-ness in a C57BL/6 mouse model of ACD using contact hyper-sensitivity (CHS) elicited by 2,4,6-trinitro-1-chlorobenzene was evaluated as a marker of inflammation level. Five and nine mice were injected with ASCs and phosphate-buffered saline (PBS), respectively. After ASC or PBS injection, re-al- time reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay were performed. Results: Histology showed that CHS was self-limited and ear thickness was suppressed by ASCs in a dose-dependent manner. IFN-γ expression in the elicited skin site and re-gional lymph nodes was significantly lower in ASC-treated mice than in control mice. IL-10 expression did not differ be-tween treated and control mice. The suppressive effects of ASCs on CHS response did not differ between IL-10 knock-out C57BL/6 mice and wild-type mice. Conclusion: The present findings suggest that MSCs in adipose tissue may contribute to the self-limiting course of ACD through de-creased expression of IFN-γ, but not through increased ex-pression of IL-10. (Ann Dermatol 29(4) 391∼399, 2017)