“…Impaired complement system activation or regulation has been observed in many dermatological diseases, such as hereditary ( 12 ) and acquired angioedema ( 13 ), cutaneous small vessel ( 14 , 15 ) and hypocomplementemic urticarial vasculitis ( 16 ), SLE ( 17 , 18 ), psoriasis ( 19 , 20 ), acne vulgaris ( 21 , 22 ) and hidradenitis suppurativa ( 23 ). Moreover, the complement system is also involved in the pathogenesis of autoimmune blistering dermatoses (AIBD), in particular the pemphigoid group, including bullous pemphigoid (BP), epidermolysis bullosa acquisita (EBA), mucous membrane pemphigoid (MMP), pemphigoid gestationis (PG), and, to a lesser degree, the pemphigus group ( 24 – 28 ). C3 deposits along the dermal-epidermal junction (DEJ) are observed in approximately 90% of patients with pemphigoid diseases (PDs) ( 29 – 32 ).…”