For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
17
views
38
references
 Top references
cited by
78
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      154
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: not found

      Tissue-Specific Differentiation of Colonic Macrophages Requires TGFβ Receptor Mediated Signalling

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Intestinal macrophages (mϕ) form one of the largest populations of mϕ in the body and are vital for the maintenance of gut homeostasis. They have several unique properties and are derived from local differentiation of classical Ly6C hi monocytes, but the factors driving this tissue-specific process are not understood. Here we have used global transcriptomic analysis to identify a unique homeostatic signature of mature colonic mϕ that is acquired as they differentiate in the mucosa. By comparing the analogous monocyte differentiation process found in the dermis, we identify TGFβ as an indispensable part of monocyte differentiation in the intestine and show that it enables mϕ to adapt precisely to the requirements of their environment. Importantly, TGFβR signalling on mϕ plays a crucial role in regulating the accumulation of monocytes in the mucosa, via mechanisms that are distinct from those used by IL10.

          Related collections

          Most cited references38

          • Record: found
          • Abstract: found
          • Article: not found

          Tissue-Resident Macrophage Ontogeny and Homeostasis.

          Florent Ginhoux, Martin Guilliams (2016)
          Defining the origins and developmental pathways of tissue-resident macrophages should help refine our understanding of the role of these cells in various disease settings and enable the design of novel macrophage-targeted therapies. In recent years the long-held belief that macrophage populations in the adult are continuously replenished by monocytes from the bone marrow (BM) has been overturned with the advent of new techniques to dissect cellular ontogeny. The new paradigm suggests that several tissue-resident macrophage populations are seeded during waves of embryonic hematopoiesis and self-maintain independently of BM contribution during adulthood. However, the exact nature of the embryonic progenitors that give rise to adult tissue-resident macrophages is still debated, and the mechanisms enabling macrophage population maintenance in the adult are undefined. Here, we review the emergence of these concepts and discuss current controversies and future directions in macrophage biology.
          Article 0 comments Cited 735 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Notch–RBP-J signaling controls the homeostasis of CD8− dendritic cells in the spleen

            Michele Caton, Matthew R Smith-Raska, Boris Reizis (2007)
            Signaling through Notch receptors and their transcriptional effector RBP-J is essential for lymphocyte development and function, whereas its role in other immune cell types is unclear. We tested the function of the canonical Notch–RBP-J pathway in dendritic cell (DC) development and maintenance in vivo. Genetic inactivation of RBP-J in the bone marrow did not preclude DC lineage commitment but caused the reduction of splenic DC fraction. The inactivation of RBP-J in DCs using a novel DC-specific deleter strain caused selective loss of the splenic CD8− DC subset and reduced the frequency of cytokine-secreting CD8− DCs after challenge with Toll-like receptor ligands. In contrast, other splenic DC subsets and DCs in the lymph nodes and tissues were unaffected. The RBP-J–deficient splenic CD8− DCs were depleted at the postprogenitor stage, exhibited increased apoptosis, and lost the expression of the Notch target gene Deltex1. In the spleen, CD8− DCs were found adjacent to cells expressing the Notch ligand Delta-like 1 in the marginal zone (MZ). Thus, canonical Notch–RBP-J signaling controls the maintenance of CD8− DCs in the splenic MZ, revealing an unexpected role of the Notch pathway in the innate immune system.
            Article 0 comments Cited 327 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Ly6C hi monocytes in the inflamed colon give rise to proinflammatory effector cells and migratory antigen-presenting cells.

              Ehud Zigmond, Chen Varol, Julia Farache … (2012)
              Ly6C(hi) monocytes seed the healthy intestinal lamina propria to give rise to resident CX(3)CR1(+) macrophages that contribute to the maintenance of gut homeostasis. Here we report on two alternative monocyte fates in the inflamed colon. We showed that CCR2 expression is essential to the recruitment of Ly6C(hi) monocytes to the inflamed gut to become the dominant mononuclear cell type in the lamina propria during settings of acute colitis. In the inflammatory microenvironment, monocytes upregulated TLR2 and NOD2, rendering them responsive to bacterial products to become proinflammatory effector cells. Ablation of Ly6C(hi) monocytes ameliorated acute gut inflammation. With time, monocytes differentiated into migratory antigen-presenting cells capable of priming naive T cells, thus acquiring hallmarks reminiscent of dendritic cells. Collectively, our results highlight cellular dynamics in the inflamed colon and the plasticity of Ly6C(hi) monocytes, marking them as potential targets for inflammatory bowel disease (IBD) therapy. Copyright © 2012 Elsevier Inc. All rights reserved.
              Article 0 comments Cited 298 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Journal
                Journal ID (nlm-journal-id): 101299742
                Journal ID (pubmed-jr-id): 35518
                Journal ID (nlm-ta): Mucosal Immunol
                Journal ID (iso-abbrev): Mucosal Immunol
                Title: Mucosal immunology
                ISSN (Print): 1933-0219
                ISSN (Electronic): 1935-3456
                Publication date Nihms-submitted: 9 January 2017
                Publication date (Electronic): 01 February 2017
                Publication date PMC-release: 01 August 2017
                Electronic Location Identifier: 10.1038/mi.2016.142
                Affiliations
                [1 ]Centre for Immunobiology, Institute of Infection, Immunity and Inflammation, College of Medicine, Veterinary Medicine and Life Sciences, University of Glasgow, UK
                [2 ]Institute of Immunology, Hannover Medical School, Hannover, Germany and Institute of Molecular Medicine, RWTH Aachen, Aachen, Germany
                [4 ]Centre d'Immunologie de Marseille-Luminy, Aix Marseille Université, INSERM, CNRS, 13288 Marseille, France
                [5 ]Genomics Facility IZKF, RWTH Aachen, Aachen, Germany
                Author notes
                Corresponding Author: Professor Allan Mowat, Centre for Immunobiology, Institute of Infection, Immunity and Inflammation, Sir Graeme Davies Building, University of Glasgow, 120 University Place, Glasgow G12 8TA, Scotland. Tel: +44 141 330 8414. Allan.Mowat@ 123456glasgow.ac.uk
                [3]

                Current address: MRC Centre for Inflammation Research, University of Edinburgh, UK

                Article
                Manuscript ID: EMS70945
                DOI: 10.1038/mi.2016.142
                PMC ID: 5417360
                PubMed ID: 28145440
                SO-VID: 33ac0362-2273-4928-8e0c-11f501882e77
                License:

                Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use: http://www.nature.com/authors/editorial_policies/license.html#terms

                History
                Categories
                Subject: Article

                ScienceOpen disciplines: Immunology
                Keywords: macrophage,colon,transforming growth factor β,differentiation,transcriptome
                Data availability:
                ScienceOpen disciplines: Immunology
                Keywords: macrophage, colon, transforming growth factor β, differentiation, transcriptome

                Comments

                Comment on this article

                scite_

                Similar content154

                See all similar

                Cited by76

                See all cited by

                Most referenced authors1,121

                See all reference authors