Ellen M. Gravallese

SPP1hi macrophages in RA synovial fibrin deposits promote tissue hyperplasia.

The paper identifies fibroblast-derived neurotrophin signaling as a driver of abnormal vascular maturation in RA synovia and shows that neurotrophin inhibitors can reverse this process.

Perivascular COMPhi fibrogenic fibroblasts expand in treatment-refractory rheumatoid arthritis synovium, where endothelial Notch signaling patterns fibroblast TGF-beta sensitivity via TGFBR3 regulation and persists despite post-treatment immune cell depletion.

The paper identifies a spatial proximity-sensing mechanism in fibroblasts that restores quiescent synovial lining during RA remission through the EGFR-CREB5 axis.

This study identifies granzyme K as a driver of a novel complement activation pathway independent of classical, lectin, or alternative pathways.

The paper develops SCENT, a method to create cell-type-specific enhancer-gene maps from single-cell multimodal data, identifying causal variants and genes for diseases.

The paper maps cell-type-specific eQTLs for HLA genes across multiple tissues and identifies dynamic regulation of HLA-DQ genes in immune cells.

The paper deconstructs RA synovium using single-cell data to identify six cell type abundance phenotypes associated with distinct inflammatory states.