Joel M. Guthridge

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.

This paper develops a serial immunohistochemistry method to detect multiple antigens on kidney biopsy slides, enabling high-dimensional single-cell spatial analysis.

The paper identifies ARID3a and CD68 as markers of activated naive B cell precursors in SLE, showing their association with autoimmunity and disease activity.

SPP1hi macrophages in RA synovial fibrin deposits promote tissue hyperplasia.

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

This study uses single-cell RNA-sequencing and spatial transcriptomics to analyze myeloid cell dynamics in lupus nephritis, showing shifts in immune responses linked to disease progression.

The paper identifies distinct genetic mechanisms for early (nuclear) and late (cellular) RNA eQTL by comparing their genomic localization and functional effects across tissues.

This study identifies persistent CD4+ T cell functional deficits in individuals with prolonged SARS-CoV-2 symptoms, characterized by low CD4 expression and impaired activation responses.

A single-cell atlas of blood and tissue samples from lupus nephritis patients and healthy controls identifies stromal and immune populations, including scar-associated macrophages, which correlate with disease activity.

The paper identifies three immunologically distinct groups in lupus nephritis patients based on blood immunophenotyping, correlating with histopathology, treatment response, and renal outcomes.

The paper identifies five SNPs in the DDX6-CXCR5 locus associated with autoimmune diseases and shows their functional effects on gene regulation in immune and epithelial cells.

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 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.