Giant Cell Arteritis (GCA) is an age-associated inflammatory disease affecting medium and large vessels and is driven by dysregulated myeloid cells. Clinical disease expression and response to treatment have been shown to be influenced by clonal hematopoiesis (CHIP) mutations. However, how these mutations program the functional state of myeloid cells in GCA remains unknown.
The primary aim of this project is to define how CHIP mutations—particularly DNMT3A and TET2—reprogram myeloid cell phenotypic and molecular states, and how this reprogramming impacts disease trajectory.
Leveraging a deeply phenotyped longitudinal cohort of patients with GCA (n = 85), we will perform bulk RNA sequencing and targeted DNA sequencing on temporal artery biopsies from a subset of 35 patients.
