Gary S. Firestein

SPP1hi macrophages in RA synovial fibrin deposits promote tissue hyperplasia.

The paper identifies epigenetic trajectories in ACPA+ individuals that predict RA development, showing dynamic methylation changes in Pre-RA compared to stable methylomes in non-converters and controls.

This study uses spatial transcriptomics to identify distinct gene expression patterns in RA synovial fibroblasts and macrophages, revealing region- and cell-type-specific roles in inflammation and adaptive immunity.

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.

The paper identifies immune alterations preceding rheumatoid arthritis onset and provides tools for dataset exploration.

The paper identifies activated lymphocyte phenotypes in individuals at risk for rheumatoid arthritis using mass cytometry and develops an immunophenotype score to distinguish these individuals from controls.

The paper identifies shared transcriptional and cell communication signatures in RA patients and at-risk individuals, showing how multiple pathogenic mechanisms contribute to disease initiation and progression.

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

The paper identifies joint-specific regulatory patterns in rheumatoid arthritis fibroblast-like synoviocytes by integrating chromatin accessibility and transcriptional data, revealing differences in proliferation, migration, and inflammation between hand and non-hand joints.

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 identifies a Neandertal introgressed haplotype in the OAS1 gene associated with increased risk of severe COVID-19 and shows it impairs SARS-CoV-2 clearance through genetic regulation of OAS1 expression.

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