Background: Actinic prurigo is a specific familial photodermatosis of uncertain pathogenesis.
Objective: Our purpose was to investigate the immunohistologic presentation of actinic prurigo to explore the involved pathomechanisms.
Methods: The present immunohistochemical study was performed on biopsy specimens from 20 Mexican patients presenting with a severe and perennial form of the disease.
Results: The dense inflammatory infiltrate was composed predominantly of helper T type 1 lymphocytes admixed with scattered B-cell lymphoid follicles and numerous dermal dendrocytes. Keratinocytes contained abundant tumor necrosis factor-alpha and calprotectin.
Conclusion: In subjects genetically predisposed to actinic prurigo, ultraviolet light may trigger excessive tumor necrosis factor-alpha production by keratinocytes whose sustained release in turn exerts its proinflammatory activity and deleterious epidermal effects. Such a cascade of events is in line with the therapeutic benefit already reported when thalidomide is used to treat actinic prurigo.