Year: 2014
Type: article
Abstract: Different subsets and/or polarized phenotypes of monocytes and macrophages may play distinct roles during the development and resolution of inflammation. Here, we demonstrate in a murine model of rheumatoid arthritis that nonclassical Ly6C(-) monocytes are required for the initiation and progression of sterile joint inflammation. Moreover, nonclassical Ly6C(-) monocytes differentiate into inflammatory macrophages (M1), which drive disease pathogenesis and display plasticity during the resolution phase. During the development of arthritis, these cells polarize toward an alternatively activated phenotype (M2), promoting the resolution of joint inflammation. The influx of Ly6C(-) monocytes and their subsequent classical and then alternative activation occurs without changes in synovial tissue-resident macrophages, which express markers of M2 polarization throughout the course of the arthritis and attenuate joint inflammation during the initiation phase. These data suggest that circulating Ly6C(-) monocytes recruited to the joint upon injury orchestrate the development and resolution of autoimmune joint inflammation.
Source: Cell Reports
Language: English
Subfield: Rheumatology
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $5,620
Funders: Rheumatology Research Foundation, Northwestern University, United States-Israel Binational Science Foundation, Versus Arthritis, National Institutes of Health, Robert H. Lurie Comprehensive Cancer Center, National Heart, Lung, and Blood Institute, National Cancer Institute, National Institute of Allergy and Infectious Diseases, National Institute of Environmental Health Sciences, National Institute of Arthritis and Musculoskeletal and Skin Diseases
Awards: G111022076, Cardiovascular Regenerative Medicine, G1444394703, G1624973845, G1882761228, G294581244, Therapeutic Role for P21 in Suppressing IL-1 Beta Mediated Pathologies, Development of a Novel RA/Atherosclerosis Mouse Model, A novel and improved mouse system for studying macrophage specific gene deletion, Caspase 8: A Novel Suppressor of Dendritic Cell-Mediated Autoimmunity, G6499134989, Signaling in the lung induced by particulate matter air pollution, Role of BH3-Domain Proteins in the Effector Phase of RA, G7473363761, The Robert H. Lurie Comprehensive Cancer Center
OpenAlex ID: W2065639597