Leakage of sweat into the dermo-epidermal junction as a possible trigger for lichen planus lesion development.

No previous studies have convincingly linked sweating disturbance with the subsequent development of lichen planus (LP). Therefore, we investigated whether sweating disturbance could be specifically detected in LP lesions and how it could trigger lesion development. We utilized the impression mold technique (IMT), which allows accurate quantification of individual sweat glands/ducts actively delivering sweat in a well-defined location, to evaluate sweating disturbance in LP lesions. Psoriasis vulgaris (PsV) lesions were included as controls. Leakage of sweat and subsequent induction of chemokine expression were immunohistochemically identified. Both baseline and thermal stimulus-induced sweating responses were markedly impaired in LP lesions, as well as in PsV lesions. A marked difference, however, was found in normal-appearing perilesional skin; "cold spots", which were defined as a 1 mm2 area with no sweat droplets, were specifically and abundantly detected in perilesional LP skin, but not perilesional PsV skin. Leakage of sweat as evidenced by the immunohistochemical detection of dermcidin was specifically observed around the acrosyringium of these "cold spots" in LP, but not PsV, lesions and associated with CXCL10 induction on neighboring keratinocytes and syringotropic migration of CXCR3+ T cells. Leakage of sweat into the dermo-epidermal junction would serve not only to decrease sweat delivery to the skin surface but also to induce T-cell recruitment to the inflammatory site. Therapies for LP may be directed not only at ameliorating inflammatory responses but also at preventing the leakage of sweat into the dermo-epidermal junction.