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Autoimmunity of Pemphigus



The long term goal of Dr. Culton’s research program is to better understand the development of mucocutaneous autoimmune disease with particular interest in autoreactive B lymphocyte development, regulation, and contribution to disease.

We are currently studying two disease models of mucocutaneous autoimmunity:

  • Pemphigus is a group of life threatening blistering autoimmune diseases of the skin and mucosa caused by autoantibodies directed against the cell adhension molecules desmoglein 1 (Dsg1) and desmoglein 3 (Dsg3). The aim of our research is to understand the development and behavior of anti-desmoglein (Dsg) B cells and the autoantibodies they eventually produce, and to clarify their role in the pathogenesis of pemphigus subtypes. We have developed a humanized Dsg3 murine model with specifically allows us to study mucosal pemphigus pathophysiology and provides a new animal model in which to test novel therapeutics.
  • Lichen planus is a cell-mediated immune disorder characterized clinically by lesions on the skin and mucosal tissues (oral, genital). Lichen planus is thought to be mediated by T lymphocytes as these cells are present in a band-like pattern in the superficial dermis in lesional skin histologically. We have begun to study triggers of erosive oral lichen planus (the most chronic and recalcitrant form of this disease) in large patient cohorts. Identifying local or systemic triggers may help us understand changes that lead to active disease and potentially elucidate the putative antigenic target(s) of the pathogenic T lymphocytes. In addition, we are interested in exploring the diagnostic accuracy and clinical relevance of histologic and immunofluorescence findings in oral lichen planus.