Melanie H. Smith

SPP1hi macrophages in RA synovial fibrin deposits promote tissue hyperplasia.

This study identifies two distinct Treg states in RA synovial tissues using scRNA-seq, showing one is dysfunctional and reversible through TNFR2 engagement.

The paper identifies a mechanism where TLR4-driven cross-presentation of citrullinated antigens by dendritic cells and autoreactive B cells activates CD8+ T cells in rheumatoid arthritis.

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.

This study identifies senescent activated naive B cells in ACPA+ individuals that promote anti-citrullinated antigen T cell responses and drive progression to clinical RA.

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

The paper uses spatial transcriptomics and a new method called DeepTopics to identify distinct cellular patterns in RA synovium, revealing divergent ectopic lymphoid structures.

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.