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Bullous systemic lupus erythematosus (BSLE) and epidermolysis bullosa acquisita (EBA) are subepidermal blistering diseases associated with autoimmunity against type VII collagen.¹ The criteria for the diagnosis of BSLE include (1) a diagnosis of systemic lupus erythematosus (SLE), (2) a nonscarring vesiculobullous eruption, (3) subepidermal blisters with a neutrophil-rich infiltrate in the papillary dermis, (4) deposition of immunoreactants at the epidermal basement membrane, and (5) immunoglobulin deposits at or beneath the lamina densa seen by immunoelectron microscopy.²

By immunofluorescence (IF) microscopy, autoantibodies binding to the dermal side of the salt-split skin have been demonstrated in patients with BSLE.¹ Bullous SLE autoantibodies recognize the noncollagenous domain 1 of type VII collagen.^3-4 Immunoreactant deposits in skin biopsy specimens of patients with BSLE were shown to recruit leukocytes and induce separation at the dermoepidermal junction, suggesting a pathogenic role of these cells for blistering in BSLE.^5-6

In EBA, the ability of patients' autoantibodies to . . . [Full Text of this Article]

Report of Cases


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AUTHOR INFORMATION
Josep E. Herrero-González, MD; José M. Mascaró, Jr, MD; Carmen Herrero, MD; Amrei Dilling, MD; Detlef Zillikens, MD; Cassian Sitaru, MD, PhD