Background/Aims: Thyroid Eye Disease (TED) is an orbital autoimmune disorder affecting ~50% of patients with Graves’ disease, causing pain, diplopia, proptosis, and, in severe cases, disfigurement or blindness. TED progresses from inflammation to fibrosis and remodeling, but mechanisms underlying this transition remain unclear. This study characterizes distinct cellular landscapes in acute and fibrotic TED, emphasizing fibroblast heterogeneity and immune interactions. METHODS Orbital tissues obtained during decompression surgery from 12 TED patients (active: Clinical Activity Score ≥3, n=6; inactive: CAS<3, n=6) and 2 non-inflammatory controls were analyzed. Single-cell RNA and V(D)J sequencing profiled cellular states and immune repertoires. RESULTS Single-cell analysis identified distinct fibroblast phenotypes linked to disease activity. Active TED showed inflammatory-adipogenic PLIN2⁺/TNFSF8⁺ fibroblasts expressing KYNU and S100A9, correlating with proptosis and inflammation. Inactive TED exhibited fibrotic (SPARC, GPX3, BAMBI) and contractile (TAGLN, NDUFA4L2, COLEC11) phenotypes associated with tissue remodeling. TCR analysis revealed CD8⁺ T cell clonal expansion in active TED, suggesting targeted cytotoxic responses. A RORA⁺ fibroblast cluster co-expressing TSHR and IGF1R may mediate stage transitions via ELL2 signaling. Differential expression analysis revealed that T cells, endothelial cells, and fibroblasts exhibited the largest transcriptional changes between active and inactive TED. T cells showed upregulation of activation and signaling genes notably REL, NFKB1, and CD69, while fibroblasts expressed inflammatory-adipogenic and extracellular matrix-related markers including PLIN2, S100A16, LPL, TNFSF8, and LAMA5. CONCLUSIONS This study delineates fibroblast and immune heterogeneity in TED, uncovering transcriptomic programs underlying inflammatory-adipogenic and fibrotic-contractile transitions. These insights provide a framework to identify stage-specific therapeutic targets and biomarkers.