Immunopathogenesis of skin injury in systemic lupus erythematosus

Purpose of review Skin injury is the most common clinical manifestation of SLE and is disfiguring, difficult to treat, and incompletely understood. We provide an overview of recently published articles covering the immunopathogenesis of skin injury in SLE Recent findings Skin of SLE has an inherent susceptibility to apoptosis, the cause of which may be multifactorial. Chronic IFN overexpression leads to barrier disruption, infiltration of inflammatory cells, cytokine production, and release of autoantigens and autoantibody production that result in skin injury. Ultraviolet light is the most important CLE trigger and amplifies this process leading to skin inflammation and potentially systemic disease flares. The pathogenesis of skin injury in CLE is complex but recent studies highlight the importance of mechanisms driving dysregulated epidermal cell death likely influenced by genetic risk factors, environmental triggers (UV light), and cytotoxic cells and cellular signaling.