Serum from patients with systemic vasculitis induces alternatively activated macrophage M2c polarization

Copyright © 2014 Elsevier Inc. All rights reserved.

Détails bibliographiques
Publié dans:Clinical immunology (Orlando, Fla.). - 1999. - 152(2014), 1-2 vom: 01. Mai, Seite 10-9
Auteur principal: Ohlsson, Susanne M (Auteur)
Autres auteurs: Linge, Carl Petrus, Gullstrand, Birgitta, Lood, Christian, Johansson, Asa, Ohlsson, Sophie, Lundqvist, Andrea, Bengtsson, Anders A, Carlsson, Fredric, Hellmark, Thomas
Format: Article en ligne
Langue:English
Publié: 2014
Accès à la collection:Clinical immunology (Orlando, Fla.)
Sujets:Journal Article Research Support, Non-U.S. Gov't ANCA IL-10 IL-12 Macrophage polarization Macrophages Systemic vasculitis Antibodies, Antineutrophil Cytoplasmic Cytokines plus... Glucocorticoids Proto-Oncogene Proteins MERTK protein, human EC 2.7.10.1 Receptor Protein-Tyrosine Kinases c-Mer Tyrosine Kinase
Description
Résumé:Copyright © 2014 Elsevier Inc. All rights reserved.
Anti-neutrophil cytoplasmic antibody associated vasculitides (AAV) are conditions defined by an autoimmune small vessel inflammation. Dying neutrophils are found around the inflamed vessels and the balance between infiltrating neutrophils and macrophages is important to prevent autoimmunity. Here we investigate how sera from AAV patients may regulate macrophage polarization and function. Macrophages from healthy individuals were differentiated into M0, M1, M2a, M2b or M2c macrophages using a standardized protocol, and phenotyped according to their expression surface markers and cytokine production. These phenotypes were compared with those of macrophages stimulated with serum from AAV patients or healthy controls. While the healthy control sera induced a M0 macrophage, AAV serum promoted polarization towards the M2c subtype. No sera induced M1, M2a or M2b macrophages. The M2c subtype showed increased phagocytosis capacity compared with the other subtypes. The M2c polarization found in AAV is consistent with previous reports of increased levels of M2c-associated cytokines
Description:Date Completed 02.07.2014
Date Revised 17.03.2022
published: Print-Electronic
Citation Status MEDLINE
ISSN:1521-7035
DOI:10.1016/j.clim.2014.02.016