Andrew D. Filer

This paper introduces VIMA, a method for analyzing spatial molecular data to identify disease-associated spatial features, showing improved performance over existing methods in simulations and real datasets.

The paper identifies four distinct synovial macrophage populations in RA models and shows conserved inflammatory responses across conditions.

SPP1hi macrophages in RA synovial fibrin deposits promote tissue hyperplasia.

This study identifies CD4+ tissue-resident memory Th17 (TRM17) cells as the main source of IL-17A in SpA synovium, showing their role in disease pathology and potential as therapeutic targets.

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.

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

The paper investigates shared and distinct functional pathogenicity of gut microbiomes in inflammatory diseases using germ-free mice colonized with human fecal samples.

This study shows Wnt signaling drives inflammation in fibroblasts of inflammatory arthritis, suggesting it as a therapeutic target.

The paper uses multi-omic spatial analysis to identify fibroblast subsets in inflamed synovium that create tissue niches influencing immune cell trafficking and inflammation resolution.

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.