Abstract
Pemphigoid diseases (PD) comprise a group of autoimmune disorders clinically characterized by (muco)-cutaneous inflammation and subepidermal blistering. PD are caused by autoantibodies targeting structural proteins of the dermal-epidermal junction. Skin-bound immune complexes trigger recruitment of myeloid cells, engagement of Fcγ receptors, and activation of specific kinases. Selective blockade of PI3K can alleviate disease manifestation in mouse models of autoimmune diseases. Here, we evaluated the treatment efficacy of parsaclisib, a selective PI3KF064 inhibitor, in in-vitro and in-vivo models of epidermolysis bullosa acquisita (EBA) and mucous membrane pemphigoid (MMP).
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