AnneMarie Brescia, MD
|Mentors:||N. Carolyn Schanen, M.D., Ph.D.
Carlos Rosé, M.D.
Juvenile Idiopathic Arthritis (JIA) is the most common rheumatic disease of childhood. There is clinical heterogeneity both in terms of number of joints involved and response to treatment, which forms the basis for classifying clinical subgroups of the disorder. Predictors of disease course have not been identified and pathogenesis of JIA has yet to be elucidated and is likely to involve a combination of cell types in the involved joint. Similar to Rheumatoid Arthritis (RA), there is joint space narrowing, periarticular osteopenia and erosion formation. Unique to JIA, however, is condylar bony hypertrophy. Our previous studies using gene expression profiling in oligoarticular JIA revealed evidence for differential expression of genes encoding protein members of the TGFb signaling pathway as well as a number of chemokines and cytokines. The goals of the proposed studies are to define the molecular mechanisms that contribute to the clinical variability and pathogenesis of JIA.
AIM 1: To identify synovial biomarkers capable of predicting disease course in JIA
Hypothesis: Gene expression profiles reflect intrinsic differences in synovial pathobiology early in disease, which dictate disease course in JIA.
AIM 2: To investigate causal significance in role of altered expression of members of the TGFb signaling pathway in the pathogenesis of JIA
Hypothesis: Dysregulation of the TGFb signaling pathway is central to the pathogenesis of JIA.