The thesis of Nika Kotnik focuses on a rare skin autoimmune disease called bullous pemphigoid (BP). It is a disease characterised by itching, nonspecific changes on the skin and tense blisters. It has a high mortality, appears mostly in the elderly and is very hard to treat.
Antibodies cause the destruction of the hemidesmosome (a structural element of the skin), which in turn causes the split between two layers of the skin, the epidermis and the dermis. This results in the fluid filled blisters, seen in the disease. However, a subset of a disease has the autoantibodies present along with the itching and, but no blistering. It is called the nonbullous pemphigoid. That is why, in my thesis, we set to discover “what makes the blister?” We compared the BP and the NBP and looked at both diseases from different angles, including genetic (mRNA), clinical, the itch and in connection with other diseases. We also looked at the cells that are most likely to be involved the process of blistering.
We have found that activated eosinophils, activated basophils and IL-31 all have a role in the blistering process, seen in BP. We have found that complement has a role in the blistering (mRNA study). We have found that IgE probably is not involved in the blistering pathogenesis. We also observed a significant connection between BP.
