Expression of JAK3, STAT2, STAT4, and STAT6 in pemphigus vulgaris
Katarzyna Juczyńska, Anna Woźniacka, Elżbieta Waszczykowska, Marian Danilewicz, Małgorzata Wągrowska‐Danilewicz, Agnieszka Żebrowska
Abstract
Pemphigus vulgaris (PV) is an autoimmune intraepidermal bullous disease with a prevalence of 0.1–0.7 per 100,000 individuals [ 1 ]. Clinical demonstration of the disease includes flaccid blisters and erosions present within both skin and mucous membranes [ 2 ]. Characteristics of the PV disease are IgG deposits localized within lesional epidermis revealed in direct immunofluorescence examination (DIF) and circulating autoantibodies present in indirect immunofluorescence (IIF). The target antigens are cadherin molecules: desmoglein (DSG) 3 and DSG 1 [ 3 ]. After attachment of antibodies to antigens, several synergistic processes take place leading to loss of cell adhesion [ 4 ]. It is suggested that both signaling-dependent and signaling-independent pathways contribute to acantholysis development [ 5 ]. All those processes occur with participation of various cytokines and chemokines, wherein elevated levels were detected in serum, blister fluid, and perilesional skin of patients with PV. Moreover, levels of some of them were found correlating with activity of PV [ 6 ].