Interleukin-26-DNA complexes promote inflammation and dermal-epidermal separation in a modified human cryosection model of bullous pemphigoid.

ABSTRACT: Bullous pemphigoid (BP) is an autoimmune disease characterized by autoantibody-mediated activation of immune cells and subepidermal blister formation. Excess amounts of extracellular DNA are produced in BP, however, it remains unclear how extracellular DNA contributes to BP pathogenesis. Here we show a possible mechanism by which interleukin (IL)-26 binds to extracellular DNA released from neutrophils and eosinophils to support DNA sensing. Patients with BP exhibited high circulating levels of IL-26, forming IL-26-DNA complexes in the upper dermis and inside the blisters. IL-26-DNA complexes played a dual role in regulating local immunity and blister formation. First, they enhanced the production of inflammatory cytokines in monocytes and neutrophils. Second, and importantly,

SUBMITTER: Mizuno Y 

PROVIDER: S-EPMC9599390 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature