Interleukin 33 is induced by tumor necrosis factor α and interferon λ in keratinocytes and contributes to allergic contact dermatitis

Background: interleukin (il) 33,a novel member of the il-1 family,is produced mainly by epithelial cells and endothelial cells in response to various types of stress,including necrosis. the effects of il-33 on the immune cells involved in allergic contact dermatitis have recently been revealed in vitro. however,in vivo,the induction mechanism and function of il-33 are not fully understood. objectives: our objectives were to investigate induction of il-33 in keratinocytes and to evaluate the functions of il-33 and its inducers in a murine model of allergic contact dermatitis. material and methods: kertr cells,a human keratinocyte cell line,were cultured with various cytokines,including tumor necrosis factor (tnf) α and interferon (ifn) λ. il-33 expression was detected using quantitative reverse transcriptase polymerase chain reaction,immunocytochemistry,and western blotting. the functions of il-33,tnf-α,and ifn-λ in allergic contact dermatitis were evaluated using a murine model. results: tnf-α and ifn-λ induced expression of il-33 mrna and protein in kertr cells. blockade of il-33 attenuated swelling in the ears of the experimental mice. similar effects were noted for blockade of tnf-α and ifn-λ in these mice. conclusions: tnf-α and ifn-λ induce expression of il-33,and il-33 produced by keratinocytes contributes to allergic contact dermatitis. blockade of il-33,tnf-α,and ifn-λ could represent novel and potent strategies to treat allergic contact dermatitis. © 2013 esmon publicidad.