Biography: Dr. Dowling is a Pediatric Rheumatology fellow at Northwestern University Feinberg School of Medicine and Ann & Robert H. Lurie Children’s Hospital of Chicago. He obtained his B.S. at Georgetown University and his M.D.-Ph.D. degree at Albert Einstein College of Medicine. His doctoral work, under the mentorship of the late Dr. Fernando Macian, defined an essential role for autophagy in CD4+ T cell antigenic responses in autoimmunity. Dr. Dowling completed his pediatric residency at Lurie Children’s Hospital, where he joined Dr. Harris Perlman’s research group.
Dr. Dowling’s research interest is in the pathogenesis and treatment of juvenile idiopathic arthritis (JIA). He is defining genetic signatures of immune cells, with a particular emphasis on monocytes and macrophages, from the synovium, the tissue that lines the inside of the joint and is the main site of disease activity in JIA. His overarching goal is to build a synovial biopsy program in JIA and leverage functional immunogenomics to predict clinical outcomes and treatment responses that will aid the development of precision medicine approaches in JIA.
Research Summary: Juvenile idiopathic arthritis (JIA) is the most common rheumatologic condition and is a major cause of childhood-onset joint damage. Despite JIA being identified more than 100 years ago, pediatric rheumatologists diagnose JIA and their specific subtypes mainly by a physical exam (for example, counting the number of arthritic joints) rather than biomarkers (such as laboratory testing). This is problematic because we cannot reliably predict which patients will have poor outcomes at time of diagnosis. As a result, treatment approaches require some degree of trial-and-error. Our goal is to identify genetic signatures of immune cells from the synovium, the tissue that lines the inside of the joint and is the main site of disease activity in JIA, that are associated with more severe illness. By obtaining reads of gene expression from cells of the synovium, we can create snapshots (so called “transcriptomic profiles”) of patients with JIA. We can then test if these transcriptomic profiles better predict clinical outcomes and treatment responses than current classifications of JIA subtypes. Achieving these aims will allow us to identify patients with JIA who are most at risk for disease complications and who require more aggressive treatment upfront. Furthermore, understanding how JIA develops at an immunogenetic level will aid the development of patient-specific targeted treatment, or a move toward precision medicine in children with arthritis.
