Michael B. Brenner

This study identifies ARID5B as a transcription factor that shifts inflammatory fibroblasts from an inflammatory to a destructive phenotype in arthritis.

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.

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.

The paper identifies a spatial proximity-sensing mechanism in fibroblasts that restores quiescent synovial lining during RA remission through the EGFR-CREB5 axis.

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.

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

This study identifies LIFR as a master amplifier of fibroblast activation in IPF, showing that blocking LIFR reduces fibrosis in ex vivo tissue.

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

The paper identifies dynamic allele-specific expression changes in T cell activation, particularly in HLA genes, showing regulatory effects linked to autoimmune risk.

Harmony alternates diversity-penalized soft clustering with cluster-specific linear correction of PCA embeddings, integrating single-cell datasets over multiple covariates and handling 500,000 cells in 7.2GB of memory.

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.

This paper establishes a protocol for preserving and analyzing single-cell transcriptomes from cryopreserved renal tissue and urine samples in lupus nephritis studies.