Interleukin-1 in human skin: dysregulation in psoriasis.
 Cytokine dysregulation is an attractive concept to explain many of the observed abnormalities in psoriasis.
 IL-1, in particular, can potentiate immune cellular activation, activate fibroblasts, and increase endothelial cell adhesiveness to leukocytes.
 Here, we review IL-1 regulation in normal and psoriatic skin in vivo in relation to normal skin and cultured keratinocytes.
 Contrary to expectations, IL-1 functional activity in psoriatic lesions is reduced, not increased, relative to normal skin.
 The reduction is attributable to the presence of IL-1 inhibitors, reduced IL-1 alpha levels, and an IL-1 beta that lacked function in T-cell assays.
 IL-1 beta protein is actually significantly increased in psoriatic lesions, but the mechanism of its non-functionality remains unclear.
 Unlike cultured keratinocytes, which accumulate large, inactive IL-1 beta precursors, both normal and psoriatic skin process IL-1 beta to a mature form.
 Novel mechanisms of post-translational processing by epidermis in vivo may generate a novel form of IL-1 beta with unknown functions.
 The marked abnormalities of IL-1 regulation in psoriatic skin suggest that this molecule may be important in normal skin homeostasis.
