Pemphigus vulgaris is an autoimmune blistering disease caused by anti-desmoglein 3 IgG autoantibodies. It is accepted that interactions between autoreactive B and T cells are key to humoral autoimmunity targeting desmoglein 3. This orchestrated process usually occurs in secondary lymphoid organs, including the spleen and lymph nodes. Thus, it seems likely that autoreactive B cells reside and produce autoantibodies in these tissues. Yuan et al. analyzed lymphocytes in the lesional skin of patients with pemphigus vulgaris using several experimental techniques and concluded that desmoglein 3-reactive B cells were present. This finding expands our understanding of the pathogenesis of pemphigus and should be considered when following the clinical course of skin lesions and thinking about adjunctive therapy.
Takahashi, H. (2017, November 1). Desmoglein 3-Reactive B Cells “Hiding” in Pemphigus Lesions. Journal of Investigative Dermatology. Elsevier B.V. https://doi.org/10.1016/j.jid.2017.07.823