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. 2012 Dec 3;7(12):e50696. doi: 10.1371/journal.pone.0050696

Figure 8. Model for PV pathogenicity.

Figure 8

Monoclonal pathogenic antibodies, such as AK23 and monovalent PV mAbs (scFv) cloned from patients, cause loss of adhesion primarily through steric hindrance, which does not require signaling through p38 MAPK. In contrast, PV IgG induce two separate pathogenic events. In addition to the steric hindrance caused by a portion of antibodies contained in PV IgG, the polyclonal nature of PV IgG causes clustering and endocytosis of Dsg3 in a p38 MAPK dependent manner.