T cells mediate autoantibody-induced cutaneous inflammation and blistering in epidermolysis bullosa acquisita

• DOI: 10.1038/srep38357
• Publication Date: 2016-12-05T10:27:40Z
• Authors: Katja Bieber; Mareike Witte; Shijie Sun; Jennifer E. Hundt; Kathrin Kalies; Sören Dräger; Anika Kasprick; Trix Twelkmeyer; Rudolf A. Manz; Peter König; Jörg Köhl; Detlef Zillikens; Ralf J. Ludwig
• Keywords: Epidermolysis bullosa acquisita

Abstract T cells are key players in autoimmune diseases by supporting the production of autoantibodies. However, their contribution to effector phase antibody-mediated dermatoses, i.e., tissue injury and inflammation skin, has not been investigated. In this paper, we demonstrate that amplify development autoantibody-induced a prototypical, organ-specific disease, namely epidermolysis bullosa acquisita (EBA) – characterized caused autoantibodies targeting type VII collagen. Specifically, show immune complex (IC)-induced depends on presence process facilitated cell receptor (TCR)γδ NKT cells. Because damage IC-induced is neutrophil-dependent, further analyze interplay between neutrophils an experimental model EBA. We only enhance neutrophil recruitment into site but also interact with lymphatic organs. Collectively, study shows antibody-induced inflammation.