Abstract
Linear IgA bullous dermatosis (LABD) is a skin autoimmune disease characterized by the linear deposition of IgA autoantibodies at the basement membrane zone (BMZ), subepidermal blisters, and neutrophil infiltration. These IgA autoantibodies specifically recognize the hemidesmosomal component BP180 (also called type XVII collagen) and its processed 120 kDa and 97 kDa extracellular regions. The main epitopes recognized by LABD IgA autoantibodies are in the NC16A domain of BP180. Since there is a lack of immune cross-reactivity between mouse and human BP180 in the NC16A domain and lack of receptors for human IgA in mice, we generated a double humanized mouse strain expressing human BP180 NC16A domain and human IgA receptor FcαRI (termed NC16A/FcαRI mice).
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