Alcohol |
• Oxidative stress causes lipid peroxidation and a decrease in endogenous antioxidants |
• Increased histamine release → vasodilation → increased migration of inflammatory cells (including mast cells) |
• Increased arachidonic acid concentration |
• Induction of inflammation by increasing CD80 and CD86 expression → increased T cell activation |
• Increase in TNFα and overexpression of TNFα converting enzyme |
|
Cigarettes |
• Free radical formation → stimulation of cell signaling pathways, i.e., mitogen-activated protein kinase (MAPK), nuclear factor jB (NF-jB), Janus kinase (JAK), and signal transducer and transcriptional protein activator (JAK-STAT) signal pathway |
• Stimulation of dendritic cells, macrophages, and keratinocytes → release of cytokines, i.e., IL-12, TNF, IL-2 and GM-CSF, which activate lymphocytes T |
• Dioxins bind to the aryl hydrocarbon receptor on Th22 and Th17 lymphocytes → IL-17 and IL-22 productionIncreased expression of HLA-Cw6, HLA-DQA1*0201 and CYP1A1 genes |