Psoriasis is an auto-immune disease of the skin that affects as much as 2–3% of the world’s population with a significant effect on quality of life.
Genetic and environmental factors lead to the constant proliferation of skin immune cells, which produce proteins called interleukins. These proteins act on the tissue and induce the symptoms we observe in psoriasis, for example thickening of the skin or reddening.
Three of these proteins (IL-17A, IL-17F and IL-22) are essential in terms of causing psoriasis, and they are produced in high amounts by a type of immune cell that resides in the skin – called gamma delta T-17 (γδT17 for short).
Researchers at DTU are looking into how these immune cells produce the disease causing proteins. They found that a protein called STAT3 is necessary for the immune cells to proliferate and produce the psoriasis-causing proteins. STAT3 interacts with DNA and changes how genes and proteins are made. Animal studies show that if STAT3 is genetically deleted from the γδT17 immune cells, then it is possible to prevent them from proliferating and making interleukins, and in effect stop causing psoriasis.
Although STAT3 is known to be an important factor in connection with psoriasis, its role in this particular cell type in the skin was elusive. The hope is that this new data will help pave the way for new psoriasis therapies by targeting the STAT3 protein. Associate Professor Vasileios Bekiaris says: “In this regard, in our future studies, in collaboration with the Universities of Vienna and Toronto and a private company, we aim to test whether blocking STAT3 from binding to DNA with drugs can prevent immune cells from causing psoriasis.”
Read the full article in EMBO Reports
Title: STAT3 but not STAT4 is critical for γδT17 cell responses and skin inflammation
Journal: EMBO reports (2019) e48647, 24 September 2019