CD4 and psoriasis: In keratinocytes, extracellular disulfide-HMGB1 facilitates the expression of IL-18 through autocrine activation of the NF-κB p65 signalling pathway and the inflammasome; subsequently, in a mouse model of imiquimod (IMQ)-induced psoriasis, the HMGB1 and IL-18 secreted from keratinocytes contribute to IL-17 production in CD4+ T cells and the development of psoriasis by binding to RAGE (51).