T helper (Th) 17 cells have recently been implicated in psoriasis pathogenesis, but mechanisms of how these cells traffic into inflamed skin are unknown. By immunostaining for interleukin (IL)-17A and IL-22, we show numerous cells present in psoriasis lesions that produce these cytokines. We next found that Th17 cytokines (IL-17A, IL-22, and tumor necrosis factor (TNF)-α) markedly increased the expression of CC chemokine ligand (CCL) 20, a CC chemokine receptor (CCR)6 ligand, in human keratinocyte monolayer and raft cultures in a dose- and time-dependent manner. Lastly, we showed in mice that subcutaneous injection with recombinant IL-17A, IL-22, or TNF-α led to the upregulation of both CCL20 and CCR6 expression in skin as well as cutaneous T-cell infiltration. Taken together, these data show that Th17 cytokines stimulate CCL20 production in vitro and in vivo, and thus provide a potential explanation of how CCR6-positive Th17 cells maintain their continual presence in psoriasis through a positive chemotactic feedback loop.

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We present a case of disseminated dermal infection caused by Trichophyton rubrum (T. rubrum). This rare variant of dermatophytosis has an atypical clinical and histopathological presentation and occurs exclusively in immunosuppressed patients. The large, broad, pleomorphic hyphae with scattered budding arthrospores in this variant of T. rubrum infection are unusual and may represent expression of dermatophyte dimorphism previously described in vitro.

"Spam disease" is a chronic, progressive skin disease of high prevalence on Satowan and is associated with taro farming and contact with World War II-era bomb craters. Histopathological and PCR data demonstrate a nontuberculous mycobacterial infection as the cause.

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