Abstract
Pemphigus is a rare and debilitating autoimmune blistering disease due to keratinocyte cell-cell detachment (acantholysis). Treatments focus on immune suppression but are often associated with severe side effects, slow onset of action and frequent clinical relapses; therefore, innovative and non-immunosuppressive therapies are needed to provide rapid, safer and long-lasting responses. Patients’ autoantibodies (PVIgG) are fundamental for initiating the pathologic mechanisms of pemphigus. We have recently demonstrated that soluble Fas Ligand (sFasL), that is massively up-regulated and released from keratinocytes upon PVIgG binding, is essential for blister formation.
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