Laura T. Donlin

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 pre-treatment naive CD4+ T cell abundance as a predictor of severe irAEs in patients receiving anti-PD-1/CTLA4 checkpoint inhibitor therapy for melanoma.

This study identifies a PGE2-cAMP axis that opposes IFN-γ regulation of TNF responses in IL-1β+ macrophages in RA and ICI-arthritis, revealing a novel regulatory mechanism for inflammatory gene expression.

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 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.

The paper identifies a common inflammatory macrophage phenotype across severe COVID-19 and other inflammatory diseases, driven by IFN-γ and TNF-α, and suggests potential therapeutic targets.

A newly identified human macrophage phenotype in RA promotes joint tissue invasiveness and shows variable responses to anti-inflammatory medications.

The paper introduces MASC, a method to identify disease-associated cell subsets in single-cell data, and finds an expanded Th1-skewed cytotoxic CD4+ T cell subset in rheumatoid arthritis.

The paper develops a low-cost microfluidic instrument for scRNA-seq and applies it to profile synovial tissue from a rheumatoid arthritis patient, identifying 16 transcriptomic clusters and fibroblast subpopulations.