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New insights into pemphigoid diseases

Pemphigus and pemphigoid diseases are organspecific autoimmune blistering diseases (AIBD), characterized and caused by autoantibodies to structural components of the skin.[1] The autoantigens targeted in pemphigus are desmoglein 1 and 3, two proteins of the desmosomal structure, while the autoantigens in pemphigoid diseases (PD) are components of the basal membrane. For example, bullous pemphigoid (BP), the most frequent PD, is characterized by autoantibodies against type XVII collagen (COL17, BP180) and BP230, and epidermolysis bullosa acquisita (EBA) is caused by autoantibodies against type VII collagen (COL7). Besides EBA, other PD, such as mucous membrane pemphigoid (MMP), can be caused by several autoantibodies, including antiBP180, antiCOL7 and/or antilaminin 332.[2] The molecular basis and structure of the targeted antigens are summarized in this Focus Theme Issue (FTI) “Pemphigoid Diseases” (PD).[3] Despite the variability of autoantigens and the associated differences in PD pathogenesis, steroids are still the backbone of treatment, contributing to the high morbidity and increased mortality of patients with PD.[4] Therefore, joint efforts of basic scientists and clinicians are required to deepen our understanding of AIBD pathogenesis, which is expected to identify and validate muchneeded novel treatment options. In fact, in recent years, basic, translational and clinical research has led to a better understanding of disease, and several novel treatments are emerging. Within the current FTI, a faculty of expert authors has come together to synthesize recent developments in AIBD and to present novel findings, with a focus on PD.