Harris Perlman

The paper identifies four distinct synovial macrophage populations in RA models and shows conserved inflammatory responses across conditions.

SPP1hi macrophages in RA synovial fibrin deposits promote tissue hyperplasia.

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 and characterizes splenic macrophage subsets in mouse and human, revealing their ontogeny, dynamics, and age-related changes.

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 profibrotic monocyte-derived alveolar macrophages as a biomarker and therapeutic target in SSc-ILD by analyzing BAL fluid and lung explants.

The paper identifies three subpopulations of tissue-resident monocyte-lineage cells in inflammatory arthritis and examines their origins and responses to synovial disruption.

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 presents lineage tracing results from 18 myeloid-specific fate-mapping models in mouse peripheral blood and synovial tissue, validating synovial macrophage identification through flow cytometry and CITE-seq.

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 identifies a systemic age-dependent transcriptome imbalance driven by transcript length across multiple species and shows its correlation with splicing factors and environmental stressors.

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

This study identifies three monocyte transcriptional subgroups in SSc patients that correlate with disease activity, particularly lung function.

Single-cell RNA-seq of lung tissue from transplant donors, fibrosis patients, and a living patient identifies cell type-specific disease-associated molecular pathways in pulmonary fibrosis.

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