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Nonclassical Ly6C(-) monocytes drive the development of inflammatory arthritis in mice.
Misharin, Alexander V; Cuda, Carla M; Saber, Rana; Turner, Jason D; Gierut, Angelica K; Haines, G Kenneth; Berdnikovs, Sergejs; Filer, Andrew; Clark, Andrew R; Buckley, Christopher D; Mutlu, Gökhan M; Budinger, G R Scott; Perlman, Harris.
Affiliation
  • Misharin AV; Division of Rheumatology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
  • Cuda CM; Division of Rheumatology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
  • Saber R; Division of Rheumatology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
  • Turner JD; Rheumatology Research Group, College of Medical and Dental Sciences, The University of Birmingham, Birmingham B15 2TT, UK.
  • Gierut AK; Division of Rheumatology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
  • Haines GK; Department of Pathology, Yale University, School of Medicine, New Haven, CT 06520, USA.
  • Berdnikovs S; Division of Allergy and Immunology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
  • Filer A; Rheumatology Research Group, College of Medical and Dental Sciences, The University of Birmingham, Birmingham B15 2TT, UK.
  • Clark AR; Rheumatology Research Group, College of Medical and Dental Sciences, The University of Birmingham, Birmingham B15 2TT, UK.
  • Buckley CD; Rheumatology Research Group, College of Medical and Dental Sciences, The University of Birmingham, Birmingham B15 2TT, UK.
  • Mutlu GM; Section of Pulmonary and Critical Care, Department of Medicine, University of Chicago, Chicago, IL 60637, USA.
  • Budinger GR; Division of Pulmonary and Critical Care, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
  • Perlman H; Division of Rheumatology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA. Electronic address: h-perlman@northwestern.edu.
Cell Rep ; 9(2): 591-604, 2014 Oct 23.
Article in En | MEDLINE | ID: mdl-25373902
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.
Subject(s)

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Arthritis, Experimental / Monocytes / Antigens, Ly Limits: Animals Language: En Journal: Cell Rep Year: 2014 Document type: Article Affiliation country: United States Country of publication: United States

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Arthritis, Experimental / Monocytes / Antigens, Ly Limits: Animals Language: En Journal: Cell Rep Year: 2014 Document type: Article Affiliation country: United States Country of publication: United States