Psoriasis is a prototype for chronic inflammatory skin disease mediated by activated T cells showing T helper type 1 (Th1)/Th17 dominance (Di Cesare et al., 2009). In lesional psoriasis, a markedly increased number of proliferating memory-type T cells has been observed, suggesting their continuous activation by lesional antigen-presenting cells (Bos et al., 1989; Morganroth et al., 1991; Chang et al., 1992). In the psoriatic dermis, populations of mature myeloid dendritic cells (DCs) are characterized by expressing DC-lysosomal-associated membrane protein (DC-LAMP/CD208), and they characteristically aggregate together with the infiltrating T cells mimicking the T-cell areas of secondary lymphoid organs (Zaba et al., 2007). These ectopic lymphoid structures have been reported in peripheral non-lymphoid tissues during local infection and inflammation (Katou et al., 2000; Page et al.,