Expression of Fas, Fas ligand, and caspase-3 in pemphigus vulgaris

Background Pemphigus vulgaris (PV) is a severe autoimmune blistering skin disease caused primarily by autoantibodies against the desmosomal cadherins, which induce loss of cell–cell adhesion. In addition to the steric hindrance and activation of the intracellular signaling theories, apoptosis has been suggested to contribute in the mechanism by which pathogenic IgG induce acantholysis. Objective To verify the role of apoptosis in the pathogenesis of PV through the detection of Fas, Fas ligand (Fas-L), and caspase-3 expression in both lesional and nonlesional skin of PV patients. Patients and methods The study included 20 PV patients and 10 healthy controls. Skin biopsy specimens were taken from the lesional skin of PV patients (group IA), nonlesional skin of PV patients (group IB), and healthy controls (group II). An immunohistochemical staining for Fas, Fas-L, and caspase-3 was carried out for all biopsy specimens. Results On comparing groups IA and IB, a statistically significant difference was found in the expression of Fas-L and caspase-3, whereas Fas expression showed no statistically significant difference between both the groups. The same findings were obtained on comparing groups IA and II. However, on comparing groups IB and II, a statistically significant difference was found only in the expression of caspase-3 and no statistically significant difference was found between both the groups in the expression of Fas and Fas-L. Conclusion The activation of proapoptotic pathways seems to be essential for blistering in PV. Activation of the components of the apoptotic signaling, including Fas, Fas-L, and caspase-3, could augment the blistering response.