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      • Record: found
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      Is Open Access

      Immunometabolism governs dendritic cell and macrophage function

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          Abstract

          In this review, O’Neill and Pearce discuss recent intriguing findings on metabolic changes regulating the function of macrophages and dendritic cells.

          Abstract

          Recent studies on intracellular metabolism in dendritic cells (DCs) and macrophages provide new insights on the functioning of these critical controllers of innate and adaptive immunity. Both cell types undergo profound metabolic reprogramming in response to environmental cues, such as hypoxia or nutrient alterations, but importantly also in response to danger signals and cytokines. Metabolites such as succinate and citrate have a direct impact on the functioning of macrophages. Immunogenicity and tolerogenicity of DCs is also determined by anabolic and catabolic processes, respectively. These findings provide new prospects for therapeutic manipulation in inflammatory diseases and cancer.

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          Most cited references38

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          Epigenetic programming of monocyte-to-macrophage differentiation and trained innate immunity.

          Sadia Saeed, Jessica Quintin, Hindrik Kerstens … (2014)
          Monocyte differentiation into macrophages represents a cornerstone process for host defense. Concomitantly, immunological imprinting of either tolerance or trained immunity determines the functional fate of macrophages and susceptibility to secondary infections. We characterized the transcriptomes and epigenomes in four primary cell types: monocytes and in vitro-differentiated naïve, tolerized, and trained macrophages. Inflammatory and metabolic pathways were modulated in macrophages, including decreased inflammasome activation, and we identified pathways functionally implicated in trained immunity. β-glucan training elicits an exclusive epigenetic signature, revealing a complex network of enhancers and promoters. Analysis of transcription factor motifs in deoxyribonuclease I hypersensitive sites at cell-type-specific epigenetic loci unveiled differentiation and treatment-specific repertoires. Altogether, we provide a resource to understand the epigenetic changes that underlie innate immunity in humans. Copyright © 2014, American Association for the Advancement of Science.
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            T cell metabolism drives immunity

            Michael D Buck, David O’Sullivan, Erika L Pearce (2015)
            Buck et al. discuss the role of lymphocyte metabolism on immune cell development and function.
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              Oxidative metabolism and PGC-1beta attenuate macrophage-mediated inflammation.

              Divya Vats, Lata Mukundan, Justin Odegaard … (2006)
              Complex interplay between T helper (Th) cells and macrophages contributes to the formation and progression of atherosclerotic plaques. While Th1 cytokines promote inflammatory activation of lesion macrophages, Th2 cytokines attenuate macrophage-mediated inflammation and enhance their repair functions. In spite of its biologic importance, the biochemical and molecular basis of how Th2 cytokines promote maturation of anti-inflammatory macrophages is not understood. We show here that in response to interleukin-4 (IL-4), signal transducer and activator of transcription 6 (STAT6) and PPARgamma-coactivator-1beta (PGC-1beta) induce macrophage programs for fatty acid oxidation and mitochondrial biogenesis. Transgenic expression of PGC-1beta primes macrophages for alternative activation and strongly inhibits proinflammatory cytokine production, whereas inhibition of oxidative metabolism or RNAi-mediated knockdown of PGC-1beta attenuates this immune response. These data elucidate a molecular pathway that directly links mitochondrial oxidative metabolism to the anti-inflammatory program of macrophage activation, suggesting a potential role for metabolic therapies in treating atherogenic inflammation.
              Article 0 comments Cited 503 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Exp Med
                Journal ID (iso-abbrev): J. Exp. Med
                Journal ID (publisher-id): jem
                Journal ID (hwp): jem
                Title: The Journal of Experimental Medicine
                Publisher: The Rockefeller University Press
                ISSN (Print): 0022-1007
                ISSN (Electronic): 1540-9538
                Publication date (Print): 11 January 2016
                Volume: 213
                Issue: 1
                Pages: 15-23
                Affiliations
                [1 ]School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College, Dublin 2, Ireland
                [2 ]Department of Immunometabolism, Max Planck Institute of Immunobiology and Epigenetics, D-79108 Freiburg, Germany
                Author notes
                Correspondence to Luke A.J. O’Neill: laoneill@ 123456tcd.ie ; or Edward J. Pearce: pearceed@ 123456ie-freiburg.mpg.de
                Article
                Publisher ID: 20151570
                DOI: 10.1084/jem.20151570
                PMC ID: 4710204
                PubMed ID: 26694970
                SO-VID: 201b7bb0-2c37-42f6-9a93-5aafb0526f93
                Copyright © © 2016 O'Neill and Pearce
                License:

                This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

                History
                Date received : 01 October 2015
                Date accepted : 16 November 2015
                Categories
                Subject: Reviews
                Subject: Review

                ScienceOpen disciplines: Medicine
                Data availability:
                ScienceOpen disciplines: Medicine

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