Pemphigus vulgaris and foliaceus IgG autoantibodies directly block heterophilic trans-interaction between desmoglein and desmocollin

Anti-desmoglein (Dsg) 1 and Dsg3 IgG autoantibodies in pemphigus foliaceus (PF) and vulgaris (PV) cause blisters through loss of desmosomal adhesion. It is controversial whether blister formation is due to direct inhibition of Dsg or intracellular signaling events causing desmosome destabilization or both. Recent studies show that heterophilic binding between Dsg and desmocollin (Dsc) is the fundamental adhesive unit of desmosomes. To eliminate cellular contributions to potential pathogenicity of pemphigus Abs, bead assays coated with recombinant Dsg1, Dsc1, Dsg3, or Dsc3 ectodomains were developed.

Source: Journal of Investigative Dermatology - March 2, 2020 Category: Dermatology Authors: Ken Ishii, Kenji Yoshida, John R. Stanley, Jun Yamagami, Masayuki Amagai, Akira Ishiko Tags: Original Article Source Type: research