Sjögren's Disease (SjD) is a chronic autoimmune disease characterized by immune mediated destruction of salivary and lacrimal glands leading to severe dry mouth and associated oral health complications, vision threatening dry eye disease, and overall reduced quality of life. Despite being one of the most common autoimmune rheumatic diseases, the immunological and molecular mechanisms of SjD remain largely unknown, with no cure or effective therapy to reverse the damage caused by the disease. Recent GWAS studies implicate a role for Tyk2, a non-receptor tyrosine kinase that is essential for signaling pathways mediated by cytokine receptors. To study SjD, we utilize the non-obese diabetic (NOD) mouse model, which spontaneously develops glandular inflammation similar to Sjögren's patients. Tyk2 KO NOD mice do not develop spontaneous glandular inflammation, but the mechanisms by which Tyk2 promotes SjD are not known. My project focuses on investigating the adaptive and innate immune mechanisms through which Tyk2 contributes to salivary gland autoimmunity in NOD mice. By understanding the role of Tyk2 in this process, we aim to identify key biomarkers that are essential for tracking disease modulation and assessing the efficacy of current Tyk2 inhibitor therapies.
 

Honors/Awards

Lulu Merle Johnson Fellowship (2023-2028)