Potential role of interleukin-17 in the pathogenesis of bullous pemphigoid

Abstract

Bullous pemphigoid is an autoimmune blistering disease of the skin caused by autoantibodies directed against basement membrane zone adhesion molecules. Autoantibodies cannot fully explain several important features of the disease such as the difficulty transferring with the pathogenic autoantibodies, or the presence of heavy lesional infiltration of eosinophils and neutrophils that is necessary for disease production. There is increasing evidence that Th17 cells and the cytokines they release such as interleukin-17 are important regulators of innate and adaptive immune responses in many Th1 and/or Th2 mediated autoimmune diseases such as rheumatoid arthritis, systemic lupus erythematosus, and allergic asthma. There is also evidence that Th17 cells have a role in pathogenesis of blistering skin diseases. Interleukin-17 is important in initiation and maintenance of many autoimmune reactions and it is involved in production of pro-inflammatory cytokines, matrix metalloproteinases, neutrophils, and eosinophils, all of which are important pathogenic factors in bullous pemphigoid. The hypothesis is that interleukin-17 has an important pathogenic role in BP and can describe features of the disease not explained by the autoantibody theory. This cytokine can be assessed in the blister fluid and sera of patients, and can be used as a marker of disease activity and response to therapy. The information obtained could also lead to the development of novel therapeutic strategies for this and other autoimmune blistering diseases.