My research explores the potential link between Dipeptidyl Peptidase 4 inhibitors (DPP4i) – a class of drugs commonly used to treat type 2 diabetes – and the development of autoimmune blistering diseases, particularly pemphigoid diseases. These diseases, including bullous pemphigoid (BP), mucous membrane pemphigoid (MMP), and epidermolysis bullosa acquisita (EBA), are marked by the formation of blisters and inflammation in the skin and mucous membranes due to the body’s immune system mistakenly attacking its own tissues, and I am specifically focusing on the BP.

While DPP4i treatments like vildagliptin are generally used to manage blood sugar in diabetic patients, recent studies have raised concerns about their potential to increase the risk of developing pemphigoid diseases, especially in older adults. Despite this, it is yet not fully discovered how these drugs contribute to disease development.

In my work, I aim to explore how DPP4i might trigger or worsen these autoimmune conditions by investigating molecular changes downstream of the relevant signaling in both animal models and patient data. By exploring how these drugs influence the molecular patterns developing the bullous pemphigoid, I hope to identify new insights into autoimmune disease processes.