Abstract
Pemphigus vulgaris is a chronic autoimmune blistering disease characterized by antibody production against Desmogleins 3 (Dsg3) and 1 (Dsg1) causing acantholysis. Increased levels of innate cytokines detected in the blister fluid suggest a role of innate immune system activity. To elucidate the discrepancy between binding of pathogenic antibodies and a lack of blister formation, we focused on the role of innate cofactors supporting acantholysis. Here, we used a dispase-based keratinocyte-dissociation assay with a human immortalized keratinocyte cell line (HaCaT) and human primary keratinocytes.
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