How does the pathophysiology in GPP differ from plaque type psoriasis?
Featuring Erin Boh, MD, PhD |
Joseph B. Chastain Chair of Dermatology
Tulane University Health Sciences Center
New Orleans, LA
Now since GPP has, as its driver, IL-36, that's a little bit different than our classic plaque psoriasis. When IL-36 is overexpressed it then will bind to the IL-36 receptor, which is on the cell surface of all of our cells and as a consequence of that, they go in and activate this innate pathway which runs through NF Kappa. B. We see elevated levels of IL-36, so you think well, “So what?”, IL-36 drives neutrophil recruitment. Neutrophils come massively and infiltrate into the dermis and the epidermis resulting in pustules. And actually those pustules then go on to become confluent lakes of puss.