Caveolin-1 (Cav-1) is a membrane protein that is essential for the formation of ﬂask-shaped membrane invaginations known as caveolae. Cav-1 regulates a variety of signaling molecules and receptors, and aberrant Cav-1 expression is involved in a variety of diseases. Our previous study revealed aberrant reduction of Cav-1 in the epidermis of psoriasis patients, which leads to enhanced phosphorylation of STAT3 and cytokine production, suggesting that decreased Cav-1 may contribute to psoriatic inflammation. Not only keratinocytes, but also immune cells are major players in psoriasis. Migrated immune cells produce a variety of effector cytokines which affect keratinocytes proliferation and induce psoriatic inflammation. 
 The purpose of this study was to determine whether Cav-1 is involved in the leucocyte function of psoriasis and investigate their role in the pathogenesis of psoriasis.
 We first determined Cav-1 expression levels in peripheral blood mononuclear cells (PBMCs) and polymorphonuclear cells (PMNs) isolated from 20 patients with psoriasis and 20 control subjects by quantitative PCR and immunoblotting. Immunocytochemistry and magnetic cell isolation were also conducted to identify which cells were aberrant on Cav-1 expression in PBMCs. 
 mRNA and protein levels of Cav-1 in PBMCs and PMNs were significantly lower in psoriasis patients than control subjects. In PBMCs, significant reduction of Cav-1 was observed in CD14 positive monocytes. In addition we assessed function of Cav-1 decreased monocytes on cytokine production and migration. Cav-1 RNA interference in isolated monocytes resulted in elevated levels of IL-1β and IL-6 under LPS stimulation, compared to control monocytes. Furthermore, a migration assay revealed that Cav-1 silenced monocytes had enhanced chemotaxis activity induced by MCP-1. 
 Our results suggest that aberrant Cav-1 expression in monocytes may be involved in the pathogenesis of psoriasis by mediating cell migration and cytokine production.

Downregulated Caveolin-1 expression in monocytes may contribute to the pathogenesis of psoriasis.