Kevin Wei

This study profiles B cell activation states using multi-omics data to identify genetic mechanisms underlying immune-mediated diseases.

This study uses spatial and single-cell transcriptomics to identify immune-stromal niches in adult-onset dermatomyositis, revealing distinct cellular and cytokine signatures associated with cancer and non-cancer lesions.

SPP1hi macrophages in RA synovial fibrin deposits promote tissue hyperplasia.

This study identifies MMP9+ CD14+ myeloid cells as key drivers of UVB-induced IFN-I-driven inflammation in cutaneous lupus and dermatomyositis through a keratinocyte-fibroblast-myeloid circuit.

The paper identifies fibroblast-derived neurotrophin signaling as a driver of abnormal vascular maturation in RA synovia and shows that neurotrophin inhibitors can reverse this process.

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.

This study uses spatial transcriptomics to identify CD8+ T cell-driven mechanisms of kidney damage in ICI-AIN, showing increased IFN-γ signaling and proinflammatory myeloid cell activation.

The paper shows that chronic exposure to oxidized phospholipids primes and activates NLRP3 via NRF2, independent of microbial cues, contributing to atherogenesis.

This study shows human synovial tissue-resident macrophages develop from monocytes guided by fibroblast-derived cues in specific spatial niches, using a novel organoid system.

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

This study identifies distinct myeloid DC subsets in synovial tissue across health and RA states, showing their roles in inflammation and tolerance.

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 shows that inhibiting lactate transporters MCT1 and MCT4 reduces myofibroblast differentiation and pulmonary fibrosis in vitro and in vivo.

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

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.

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

The paper identifies two distinct fibroblast subsets in arthritis that drive inflammation or tissue damage, showing their unique roles in disease progression.