My research focuses on inflammatory skin diseases in which aberrant fibroblast biology, dysfunctional extracellular matrix remodeling, and dysregulated stromal–immune interactions drive tissue fibrosis. One such disease is hidradenitis suppurativa (HS), a chronic inflammatory disease of the hair follicle characterized by painful nodules, abscesses, and draining tunnels in apocrine gland-bearing skin. In advanced HS, extensive dermal fibrosis and tunnel formation lead to permanent tissue destruction. Fibrotic skin diseases share key pathological features, such as the expansion of pro-fibrotic fibroblast subpopulations (e.g., CTHRC1+), deposition of aberrant ECM proteins (e.g., tenascin-C D domain), dense immune infiltration, and disruption of cell-cell signaling networks (e.g., stromal-immune, epithelial-immune interactions). I hope to use spatial multi-omic technologies, as well as pharmacologic and transgenic mouse models to interrogate the molecular factors, cellular subpopulations, and larger-scale cellular interactions central to HS and other chronic fibrosing skin conditions such as scleroderma. Longer term, these experiments will inform molecular and cellular therapies to prevent and perhaps even reverse existing cutaneous fibrosis.