Please use this identifier to cite or link to this item:http://hdl.handle.net/20.500.12105/6870
Phagocytosis imprints heterogeneity in tissue-resident macrophages
A-Gonzalez, Noelia CNIC | Quintana, Juan A. CNIC | García-Silva, Susana | Mazariegos, Marina | Gonzalez de la Aleja, Arturo CNIC | Nicolas-Avila, Jose A. CNIC | Walter, Wencke CNIC | Adrover, Jose M CNIC | Crainiciuc, Georgiana CNIC | Kuchroo, Vijay K | Rothlin, Carla V | Peinado Selgas , Hector CNIO | Castrillo, Antonio | Ricote, Mercedes CNIC | Hidalgo, Andrés CNIC
J Exp Med. 2017; 214(5):1281-1296
Tissue-resident macrophages display varying phenotypic and functional properties that are largely specified by their local environment. One of these functions, phagocytosis, mediates the natural disposal of billions of cells, but its mechanisms and consequences within living tissues are poorly defined. Using a parabiosis-based strategy, we identified and isolated macrophages from multiple tissues as they phagocytosed blood-borne cellular material. Phagocytosis was circadianally regulated and mediated by distinct repertoires of receptors, opsonins, and transcription factors in macrophages from each tissue. Although the tissue of residence defined the core signature of macrophages, phagocytosis imprinted a distinct antiinflammatory profile. Phagocytic macrophages expressed CD206, displayed blunted expression of Il1b, and supported tissue homeostasis. Thus, phagocytosis is a source of macrophage heterogeneity that acts together with tissue-derived factors to preserve homeostasis.
Interleukin-1beta | Lectins, C-Type | Macrophages | Male | Mannose-Binding Lectins | Mice | Opsonin Proteins | Phagocytosis | Receptors, Cell Surface | Transcription Factors
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