Dr. Skaug provides Rheumatology care and consultation at the UT Professional Building and Memorial Hermann Hospital in the Texas Medical Center and at Lyndon Baines Johnson Hospital within the Harris Health system. Being both an MD and PhD gives Dr Skaug the ability to see the real-life applications of research, giving him unique insight into what this condition means to the patients that have it. Understanding what gaps in our knowledge mean for those with autoimmune conditions inspires this physician and researches to keep pushing for answers that will lead to improved treatments and maybe even a cure.
Dr Skaug’s research is focused on identifying mechanisms that drive dysfunction of the immune system in the autoimmune disease scleroderma. Scleroderma is a disease that affects connective tissues, resulting in thickening of the skin, scar tissue on organs such as the lungs and kidneys and thickening of blood vessels leading to high blood pressure and tissue damage.
Previous research in the division identified dysfunction of a gene, DNASE1L3, as a risk factor for developing scleroderma. Dysfunction of this gene appears to be a risk factor for multiple autoimmune diseases including systemic sclerosis, lupus, vasculitis, and rheumatoid arthritis, suggesting that DNASE1L3 is important for maintaining proper function of the immune system.
Results from research conducted in his first year as an ANRF scholar supports the hypothesis that this scleroderma-associated genetic variant impairs the ability of DNASE1L3 to clear the DNA from cells that have died during normal cell turnover. Given this progress Dr Skaug was awarded a second year of funding.
“The focus of my research for the second year is to determine how this excess DNA contributes to the imbalanced immune system commonly observed in scleroderma patients. This work will include searching for the cell types that interact with this excess DNA and determining the downstream effects of this DNA on immune cell function. Completion of this work could help us understand a mechanism underlying the excess immune cell activity observed in systemic sclerosis and other autoimmune diseases.”