학술논문

Defining inflammatory cell states in rheumatoid arthritis joint synovial tissues by integrating single-cell transcriptomics and mass cytometry
Document Type
article
Source
Nature Immunology. 20(7)
Subject
Clinical Research
Autoimmune Disease
Arthritis
Human Genome
Rheumatoid Arthritis
Genetics
Aetiology
2.1 Biological and endogenous factors
Inflammatory and immune system
Good Health and Well Being
Arthritis
Rheumatoid
Autoimmunity
Biomarkers
Computational Biology
Cross-Sectional Studies
Cytokines
Fibroblasts
Flow Cytometry
Gene Expression
Gene Expression Profiling
High-Throughput Nucleotide Sequencing
Histocompatibility Antigens Class II
Humans
Leukocytes
Monocytes
Signal Transduction
Single-Cell Analysis
Synovial Membrane
T-Lymphocyte Subsets
Transcriptome
Workflow
Accelerating Medicines Partnership Rheumatoid Arthritis and Systemic Lupus Erythematosus (AMP RA/SLE) Consortium
Immunology
Language
Abstract
To define the cell populations that drive joint inflammation in rheumatoid arthritis (RA), we applied single-cell RNA sequencing (scRNA-seq), mass cytometry, bulk RNA sequencing (RNA-seq) and flow cytometry to T cells, B cells, monocytes, and fibroblasts from 51 samples of synovial tissue from patients with RA or osteoarthritis (OA). Utilizing an integrated strategy based on canonical correlation analysis of 5,265 scRNA-seq profiles, we identified 18 unique cell populations. Combining mass cytometry and transcriptomics revealed cell states expanded in RA synovia: THY1(CD90)+HLA-DRAhi sublining fibroblasts, IL1B+ pro-inflammatory monocytes, ITGAX+TBX21+ autoimmune-associated B cells and PDCD1+ peripheral helper T (TPH) cells and follicular helper T (TFH) cells. We defined distinct subsets of CD8+ T cells characterized by GZMK+, GZMB+, and GNLY+ phenotypes. We mapped inflammatory mediators to their source cell populations; for example, we attributed IL6 expression to THY1+HLA-DRAhi fibroblasts and IL1B production to pro-inflammatory monocytes. These populations are potentially key mediators of RA pathogenesis.