Illicium verum extract inhibits TNF-α- and IFN-γ-induced expression of chemokines and cytokines in human keratinocytes

Xanthii fructus extract inhibits TNF-α/IFN-γ-induced Th2-chemokines production via blockade of NF-κB, STAT1 and p38-MAPK activation in human epidermal keratinocytes

“…AD is commonly characterized by infiltration of Th2-type lymphocytes into skin lesions and is known to be associated with high levels of chemokines like thymus and activation-regulated chemokine (TARC/CCL17) and macrophage-derived chemokine (MDC/CCL22) (Shimada et al, 2004). TARC/CCL17 and MDC/CCL22 are members of the CC chemokine subfamily and are produced by keratinocytes, endothelial cells, and monocyte-derived dendritic cells (Sung et al, 2012). CC chemokine receptor 4 (CCR4) is the specific receptor for TARC and MDC, and is predominantly expressed on Th2 lymphocytes (Kwon et al, 2012).…”

Phloretin ameliorates chemokines and ICAM-1 expression via blocking of the NF-κB pathway in the TNF-α-induced HaCaT human keratinocytes

“…Previous observations found that keratinocytes from skin of patients with atopic dermatitis could secrete more proinflammatory cytokines and chemokines to cause skin leagen [5]. An earlier study found that human keratinocytes stimulated with TNF-α could induce cytokine production and the expression of chemokines, such as IL-8, MCP-1, TARC, and MDC, to involve immune and inflammatory responses in skin during atopic dermatitis [4,20].…”

“…TARC could bind to the chemokine receptor CCR4 of T cells and induce monocyte activation [30]. In atopic dermatitis patients, MDC could induce Th2 cell migration and activate Th2 cells to secrete Th2-type cytokines, such as IL-4, IL-5, and IL-13 [4,20]. However, MDC inhibited activity of Th1 cells and downregulated Th1-type cytokines [5].…”

Effect of isosecotanapartholide isolated from Artemisia princeps Pampanini on IL-33 production and STAT-1 activation in HaCaT keratinocytes

“…Previous studies reported that TNF-α/IFN-γ stimulation activates signaling molecules, including STAT-1, extracellular signal-regulated kinase, c-Jun N-terminal kinase, p38 mitogen-activated protein kinases (MAPKs) and nuclear factor (NF)-κB in HaCaT cells (26)(27)(28)(29)(30). Thus, the present study evaluated whether ISTP affects the STAT signaling pathway in TNF-α/IFN-γ-stimulated HaCaT cells using western blot analysis.…”