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Epidermal desquamation is the highly regulated process of invisible shedding of corneocytes from the outermost layers of the stratum corneum. This occurs through the interplay between proteases and their inhibitors that control the degradation of corneodesmosomes. Skin peeling refers to exaggerated visible superficial desquamation and can occur in inherited and acquired conditions. The illumination of the molecular basis of genetic disorders with skin peeling sheds light on the biological mechanisms of epidermal desquamation and skin barrier homeostasis.
The SATB1 protein has been the focus of two recent studies of cutaneous T-cell lymphomas. Fredholm et al. observed a stage-related decrease of SATB1 expression in epidermotropic cutaneous T-cell lymphomas. SATB1 was negatively regulated by STAT5 through microRNA-155, which in turn triggered enhanced expression of T helper type 2 cytokines such as IL-5 and IL-9. In parallel, Sun et al. found that SATB1 expression was up-regulated by promoter demethylation in a subset of cutaneous anaplastic lymphoma and was associated with T helper type 17 polarization in patients with better therapeutic responses.
The cytokine IL-17 plays a critical role in host defense against fungal infections. So far, clinical relevance for IL-17 antifungal activity focused on mucocutaneous candidiasis. Burstein and colleagues now provide evidence that type 17 immunity is also essential for defense against dermatophytosis.
Pandeya et al. report that nevus-associated melanoma is associated with a specific phenotype, namely, young age, high number of nevi, non-brown eye color and slight dermal elastosis. Potential implications regarding differences between nevus-associated melanomas and de novo melanomas are discussed.