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ABSTRACT: Background
A better understanding of the pathogenesis of polyarticular juvenile idiopathic arthritis (polyJIA) is needed to aide in the development of data-driven approaches to guide selection between therapeutic options. One inflammatory pathway of interest is JAK-STAT signaling. STAT3 is a transcription factor critical to the differentiation of inflammatory T helper 17 cells (Th17s). Previous studies have demonstrated increased STAT3 activation in adult patients with rheumatoid arthritis, but less is known about STAT3 activation in polyJIA. We hypothesized that Th17 cells and STAT3 activation would be increased in treatment-naïve polyJIA patients compared to pediatric controls.Methods
Blood from 17 patients with polyJIA was collected at initial diagnosis and again if remi
SUBMITTER: Wood S
PROVIDER: S-EPMC10908086 | biostudies-literature | 2024 Mar
REPOSITORIES: biostudies-literature