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      Trained immunity: a program of innate immune memory in health and disease

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          Abstract

          The general view that only adaptive immunity can build immunological memory has recently been challenged. In organisms lacking adaptive immunity as well as in mammals, the innate immune system can mount resistance to reinfection, a phenomenon termed trained immunity or innate immune memory. Trained immunity is orchestrated by epigenetic reprogramming, broadly defined as sustained changes in gene expression and cell physiology that do not involve permanent genetic changes such as mutations and recombination, which are essential for adaptive immunity. The discovery of trained immunity may open the door for novel vaccine approaches, for new therapeutic strategies for the treatment of immune deficiency states, and for modulation of exaggerated inflammation in autoinflammatory diseases.

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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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            Candida albicans infection affords protection against reinfection via functional reprogramming of monocytes.

            Jessica Quintin, Sadia Saeed, Joost H.A. Martens … (2012)
            Immunological memory in vertebrates is often exclusively attributed to T and B cell function. Recently it was proposed that the enhanced and sustained innate immune responses following initial infectious exposure may also afford protection against reinfection. Testing this concept of "trained immunity," we show that mice lacking functional T and B lymphocytes are protected against reinfection with Candida albicans in a monocyte-dependent manner. C. albicans and fungal cell wall β-glucans induced functional reprogramming of monocytes, leading to enhanced cytokine production in vivo and in vitro. The training required the β-glucan receptor dectin-1 and the noncanonical Raf-1 pathway. Monocyte training by β-glucans was associated with stable changes in histone trimethylation at H3K4, which suggests the involvement of epigenetic mechanisms in this phenomenon. The functional reprogramming of monocytes, reminiscent of similar NK cell properties, supports the concept of "trained immunity" and may be employed for the design of improved vaccination strategies. Copyright © 2012 Elsevier Inc. All rights reserved.
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              Innate immunity of the newborn: basic mechanisms and clinical correlates.

              Ofer Levy (2007)
              The fetus and newborn face a complex set of immunological demands, including protection against infection, avoidance of harmful inflammatory immune responses that can lead to pre-term delivery, and balancing the transition from a sterile intra-uterine environment to a world that is rich in foreign antigens. These demands shape a distinct neonatal innate immune system that is biased against the production of pro-inflammatory cytokines. This bias renders newborns at risk of infection and impairs responses to many vaccines. This Review describes innate immunity in newborns and discusses how this knowledge might be used to prevent and treat infection in this vulnerable population.
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                Author and article information

                Journal
                Journal ID (nlm-journal-id): 0404511
                Journal ID (pubmed-jr-id): 7473
                Journal ID (nlm-ta): Science
                Journal ID (iso-abbrev): Science
                Title: Science (New York, N.Y.)
                ISSN (Print): 0036-8075
                ISSN (Electronic): 1095-9203
                Publication date Nihms-submitted: 24 October 2016
                Publication date (Electronic): 21 April 2016
                Publication date (Print): 22 April 2016
                Publication date PMC-release: 22 April 2017
                Volume: 352
                Issue: 6284
                Page: aaf1098
                Affiliations
                [1 ]Department of Internal Medicine and Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen, The Netherlands
                [2 ]Institute of Innate Immunity, Bonn University, Bonn, Germany
                [3 ]Department of Infectious Diseases and Immunology, UMass Medical School, Worcester, MA, USA
                [4 ]German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany
                [5 ]School of Biochemistry and Immunology, Trinity College, Dublin, Ireland
                [6 ]Department of Experimental Oncology, European Institute of Oncology, Milan, Italy
                [7 ]Radboud University, Department of Molecular Biology, Faculties of Science and Medicine, and Radboud Institute of Molecular Life Sciences, Nijmegen, The Netherlands
                [8 ]The Broad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, MA, USA
                [9 ]Center for Computational and Integrative Biology and Gastrointestinal Unit, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA
                Author notes
                [* ] Correspondence: Mihai G. Netea, M.D., Ph.D., Department of Internal Medicine (463), Radboud University Nijmegen Medical Centre, Geert Grooteplein Zuid 8, 6525 GA Nijmegen, The Netherlands, Tel: +31-24-3618819; Fax: +31-24-3541734, mihai.netea@ 123456radboudumc.nl
                Article
                Accession ID: PMC5087274 Pmcid ID: PMC5087274 Pmc-uid ID: 5087274 Manuscript ID: nihpa824693
                DOI: 10.1126/science.aaf1098
                PMC ID: 5087274
                PubMed ID: 27102489
                SO-VID: 31fc097f-d2c9-463e-a6fe-71fd98630275
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