Pemphigus foliaceus IgG causes dissociation of desmoglein 1–containing junctions without blocking desmoglein 1 transinteraction
J. Clin. Invest. Jens Waschke, et al. 115:3157 doi:10.1172/JCI23475 [Go to this article.]

Figure 2
PF-IgG–induced cell dissociation in HaCaT monolayers. HaCaT cells double-stained for F-actin using Alexa-phalloidin (A, D, G, J, M, and P) and Dsg3 (B, E, H, K, N, and Q). In controls, F-actin and the desmosomal cadherin Dsg3 were distributed along cell junctions (A–C). Control IgGs (35 μg/ml, 24 hours) did not affect distribution of Dsg3 (E and F). In contrast, PF1-IgGs (35 μg/ml, 24 hours) induced intercellular gaps (arrows) best seen in the Alexa-phalloidin stain for F-actin (G and I). Note that Dsg3 is still present in cell processes spanning gaps (arrowheads in H). Following immunoabsorption of PF-IgGs by Dsg1-Fc–coated beads, PF2-IgGs (35 μg/ml, 24 hours) had no effect (J–L) whereas large gaps (arrows) were induced by incubation with PF2-IgGs when control absorption was performed with beads coated with VE-cadherin–Fc (VE-Fc) (M–O), indicating requirement of autoantibodies specific for Dsg1 for cell dissociation. Note that the inhibitory monoclonal antibody directed against the extracellular domain of Dsg1 did not induce gaps (P–R). Scale bar: 40 μm for all panels (n = 5). abs., immunoabsorption.