Accelerating Medicines Partnership RA/SLE Network

This study defines the single-cell landscape of Class II lupus nephritis and identifies fibroblast transcriptional programs and chronicity index as potential predictors of kidney outcomes.

The paper identifies spatially distinct macrophage-fibroblast interactions in lupus nephritis that drive myofibroblast heterogeneity and fibrosis.

The paper uses serum proteomics to identify molecular signatures that classify lupus nephritis, differentiate disease activity and chronicity, and predict treatment response.

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

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