Blisters develop when layers of skin separate and fill with fluid as a result of external damage, drug reactions, congenital conditions or an auto-immune response. In autoimmune skin blistering diseases, antibodies mistakenly attack proteins that are essential for the layers of skin to stick together, forming blisters that can cover a significant portion of the skin. This can compromise the skin’s ability to function as a barrier and temperature regulator and, depending on size and severity, can be fatal.
In research funded in part by the Michael Smith Foundation for Health Research (MSFHR) and published in Nature Scientific Reports, Granville, post-doctoral fellow Dr. Valerio Russo, and a team that includes MSFHR Research Trainees Drs. Nestor Solis and Matthew Zeglinski, identify an enzyme which is responsible for the disruption of the skin’s basement membrane and the resulting epidermal detachment and blistering.
