Pemphigus: An Autoimmune Disease Model for Understanding the Role of Autoreactive T Cells

Abstract

Finding cures is the ultimate goal of research on autoimmune diseases. Pemphigus is an autoantibody-mediated autoimmune skin disease in which specific autoantibodies target desmogleins 1 and 3 as autoantigens. The condition leads to painful blisters and erosions in the skin and oral mucosa, impacting patients’ ability to eat and other daily activities, significantly affecting quality of life. The molecular mechanisms by which these pathogenic autoantibodies induce blisters have been extensively studied and understanding has advanced considerably. However, many critical questions remain, such as the exact cause of the disease, the mechanisms that normally prevent autoimmunity, and the pathogenic cells involved, other than autoantibodies. This article focuses on the role of autoreactive T cells in pemphigus and uses the pemphigus model to answer some of these questions. Research into pemphigus has enhanced our understanding of both the pathogenic and regulatory mechanisms involved, not only in pemphigus but also in other skin diseases caused by cellular autoimmunity. The growing body of scientific evidence on pemphigus has made it a model disease, paving the way for the development of novel therapeutic approaches, including antigen-specific immunotherapy for autoimmune diseases and chronic inflammatory disorders.