Defining inflammatory cell states in rheumatoid arthritis joint synovial tissues by integrating single-cell transcriptomics and mass cytometry.

Zhang, Fan, Wei, Kevin, Slowikowski, Kamil, Fonseka, Chamith Y, Rao, Deepak A, Kelly, Stephen, Goodman, Susan M, Tabechian, Darren, Hughes, Laura B, Salomon-Escoto, Karen, Watts, Gerald F M, Jonsson, A Helena, Rangel-Moreno, Javier, Meednu, Nida, Rozo, Cristina, Apruzzese, William, Eisenhaure, Thomas M, Lieb, David J, Boyle, David L, Mandelin, Arthur M, Boyce, Brendan F, DiCarlo, Edward, Gravallese, Ellen M, Gregersen, Peter K, Moreland, Larry, Firestein, Gary S, Hacohen, Nir, Nusbaum, Chad, Lederer, James A, Perlman, Harris, Pitzalis, Costantino, Filer, Andrew, Holers, V Michael, Bykerk, Vivian P, Donlin, Laura T, Anolik, Jennifer H, Brenner, Michael B and Raychaudhuri, Soumya (2019) Defining inflammatory cell states in rheumatoid arthritis joint synovial tissues by integrating single-cell transcriptomics and mass cytometry. Nature immunology. ISSN 1529-2916. This article is available to all UHB staff and students via ASK Discovery tool http://tinyurl.com/z795c8c by using their UHB Athens login IDs

Full text not available from this repository.
Official URL: https://www.nature.com/articles/s41590-019-0378-1

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-DRA sublining fibroblasts, IL1B pro-inflammatory monocytes, ITGAXTBX21 autoimmune-associated B cells and PDCD1 peripheral helper T (T) cells and follicular helper T (T) 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 THY1HLA-DRA fibroblasts and IL1B production to pro-inflammatory monocytes. These populations are potentially key mediators of RA pathogenesis.

Item Type: Article
Additional Information: This article is available to all UHB staff and students via ASK Discovery tool http://tinyurl.com/z795c8c by using their UHB Athens login IDs
Subjects: QW Microbiology. Immunology
WE Musculoskeletal. Orthopaedics
Divisions: Ambulatory Care > Rheumatology
Related URLs:
Depositing User: Mr Philip O'Reilly
Date Deposited: 15 May 2019 09:40
Last Modified: 15 May 2019 09:40
URI: http://www.repository.uhblibrary.co.uk/id/eprint/2105

Actions (login required)

View Item View Item