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      The function and regulation of TET2 in innate immunity and inflammation

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          Abstract

          TET2, a member of ten-eleven translocation (TET) family as α-ketoglutarate- and Fe 2+-dependent dioxygenase catalyzing the iterative oxidation of 5-methylcytosine (5mC), has been widely recognized to be an important regulator for normal hematopoiesis especially myelopoiesis. Mutation and dysregulation of TET2 contribute to the development of multiple hematological malignancies. Recent studies reveal that TET2 also plays an important role in innate immune homeostasis by promoting DNA demethylation or independent of its enzymatic activity. Here, we focus on the functions of TET2 in the initiation and resolution of inflammation through epigenetic regulation and signaling network. In addition, we highlight regulation of TET2 at various molecular levels as well as the correlated inflammatory diseases, which will provide the insight to intervene in the pathological process caused by TET2 dysregulation.

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          Origin and physiological roles of inflammation.

          Ruslan Medzhitov (2008)
          Inflammation underlies a wide variety of physiological and pathological processes. Although the pathological aspects of many types of inflammation are well appreciated, their physiological functions are mostly unknown. The classic instigators of inflammation - infection and tissue injury - are at one end of a large range of adverse conditions that induce inflammation, and they trigger the recruitment of leukocytes and plasma proteins to the affected tissue site. Tissue stress or malfunction similarly induces an adaptive response, which is referred to here as para-inflammation. This response relies mainly on tissue-resident macrophages and is intermediate between the basal homeostatic state and a classic inflammatory response. Para-inflammation is probably responsible for the chronic inflammatory conditions that are associated with modern human diseases.
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            Functions of DNA methylation: islands, start sites, gene bodies and beyond.

            Peter A. Jones (2012)
            DNA methylation is frequently described as a 'silencing' epigenetic mark, and indeed this function of 5-methylcytosine was originally proposed in the 1970s. Now, thanks to improved genome-scale mapping of methylation, we can evaluate DNA methylation in different genomic contexts: transcriptional start sites with or without CpG islands, in gene bodies, at regulatory elements and at repeat sequences. The emerging picture is that the function of DNA methylation seems to vary with context, and the relationship between DNA methylation and transcription is more nuanced than we realized at first. Improving our understanding of the functions of DNA methylation is necessary for interpreting changes in this mark that are observed in diseases such as cancer.
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              Conversion of 5-methylcytosine to 5-hydroxymethylcytosine in mammalian DNA by MLL partner TET1.

              Mamta Tahiliani, Kian Peng Koh, Yinghua Shen … (2009)
              DNA cytosine methylation is crucial for retrotransposon silencing and mammalian development. In a computational search for enzymes that could modify 5-methylcytosine (5mC), we identified TET proteins as mammalian homologs of the trypanosome proteins JBP1 and JBP2, which have been proposed to oxidize the 5-methyl group of thymine. We show here that TET1, a fusion partner of the MLL gene in acute myeloid leukemia, is a 2-oxoglutarate (2OG)- and Fe(II)-dependent enzyme that catalyzes conversion of 5mC to 5-hydroxymethylcytosine (hmC) in cultured cells and in vitro. hmC is present in the genome of mouse embryonic stem cells, and hmC levels decrease upon RNA interference-mediated depletion of TET1. Thus, TET proteins have potential roles in epigenetic regulation through modification of 5mC to hmC.
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                Author and article information

                Contributors
                Xuetao Cao: caoxt@immunol.org
                Journal
                Journal ID (nlm-ta): Protein Cell
                Journal ID (iso-abbrev): Protein Cell
                Title: Protein & Cell
                Publisher: Higher Education Press (Beijing )
                ISSN (Print): 1674-800X
                ISSN (Electronic): 1674-8018
                Publication date (Electronic): 21 October 2020
                Publication date PMC-release: 21 October 2020
                Publication date (Print): March 2021
                Volume: 12
                Issue: 3
                Pages: 165-173
                Affiliations
                [1 ]GRID grid.216938.7, ISNI 0000 0000 9878 7032, Laboratory of Immunity and Inflammation, College of Life Sciences, , Nankai University, ; Tianjin, 300071 China
                [2 ]National Key Laboratory of Medical Immunology, Institute of Immunology, Navy Military Medical University, Shanghai, 200433 China
                [3 ]GRID grid.506261.6, ISNI 0000 0001 0706 7839, Department of Immunology, Center for Immunotherapy, Institute of Basic Medical Sciences, , Chinese Academy of Medical Sciences, ; Beijing, 100005 China
                Article
                Publisher ID: 796
                DOI: 10.1007/s13238-020-00796-6
                PMC ID: 7895883
                PubMed ID: 33085059
                SO-VID: 21cd677b-0645-4e77-bc99-d0ab9a045251
                Copyright © © The Author(s) 2020
                License:

                Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

                History
                Date received : 7 July 2020
                Date accepted : 15 September 2020
                Categories
                Subject: Review
                Custom metadata
                issue-copyright-statement © The Author(s) 2021

                Keywords: tet2,innate immune response,dna demethylation,inflammatory resolution,inflammatory diseases
                Data availability:
                Keywords: tet2, innate immune response, dna demethylation, inflammatory resolution, inflammatory diseases

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