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  1. Artikel ; Online: TET Enzymes and 5hmC in Adaptive and Innate Immune Systems.

    Lio, Chan-Wang J / Rao, Anjana

    Frontiers in immunology

    2019  Band 10, Seite(n) 210

    Abstract: DNA methylation is an abundant and stable epigenetic modification that allows inheritance of information from parental to daughter cells. At active genomic regions, DNA methylation can be reversed by TET (Ten-eleven translocation) enzymes, which are ... ...

    Abstract DNA methylation is an abundant and stable epigenetic modification that allows inheritance of information from parental to daughter cells. At active genomic regions, DNA methylation can be reversed by TET (Ten-eleven translocation) enzymes, which are responsible for fine-tuning methylation patterns. TET enzymes oxidize the methyl group of 5-methylcytosine (5mC) to yield 5-hydroxymethylcytosine (5hmC) and other oxidized methylcytosines, facilitating both passive and active demethylation. Increasing evidence has demonstrated the essential functions of TET enzymes in regulating gene expression, promoting cell differentiation, and suppressing tumor formation. In this review, we will focus on recent discoveries of the functions of TET enzymes in the development and function of lymphoid and myeloid cells. How TET activity can be modulated by metabolites, including vitamin C and 2-hydroxyglutarate, and its potential application in shaping the course of immune response will be discussed.
    Mesh-Begriff(e) 5-Methylcytosine/analogs & derivatives ; 5-Methylcytosine/metabolism ; Adaptive Immunity/genetics ; Animals ; Biomarkers ; Cell Differentiation/genetics ; Cell Differentiation/immunology ; DNA Methylation ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Enzymes/genetics ; Enzymes/metabolism ; Epigenesis, Genetic ; Gene Expression Regulation ; Humans ; Immunity, Innate/genetics ; Lymphocyte Subsets/immunology ; Lymphocyte Subsets/metabolism ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/metabolism
    Chemische Substanzen Biomarkers ; DNA-Binding Proteins ; Enzymes ; Proto-Oncogene Proteins ; 5-hydroxymethylcytosine (1123-95-1) ; 5-Methylcytosine (6R795CQT4H)
    Sprache Englisch
    Erscheinungsdatum 2019-02-12
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2019.00210
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: PRMT5 Promotes T follicular helper Cell Differentiation and Germinal Center Responses during Influenza Virus Infection.

    Read, Kaitlin A / Amici, Stephanie A / Farsi, Sadaf / Cutcliffe, Madeline / Lee, Bella / Lio, Chan-Wang Jerry / Wu, Hsin-Jung Joyce / Guerau-de-Arellano, Mireia / Oestreich, Kenneth J

    Journal of immunology (Baltimore, Md. : 1950)

    2024  Band 212, Heft 9, Seite(n) 1442–1449

    Abstract: Protein arginine methyltransferases (PRMTs) modify diverse protein targets and regulate numerous cellular processes; yet, their contributions to individual effector T cell responses during infections are incompletely understood. In this study, we ... ...

    Abstract Protein arginine methyltransferases (PRMTs) modify diverse protein targets and regulate numerous cellular processes; yet, their contributions to individual effector T cell responses during infections are incompletely understood. In this study, we identify PRMT5 as a critical regulator of CD4+ T follicular helper cell (Tfh) responses during influenza virus infection in mice. Conditional PRMT5 deletion in murine T cells results in an almost complete ablation of both Tfh and T follicular regulatory populations and, consequently, reduced B cell activation and influenza-specific Ab production. Supporting a potential mechanism, we observe elevated surface expression of IL-2Rα on non-T regulatory effector PRMT5-deficient T cells. Notably, IL-2 signaling is known to negatively impact Tfh differentiation. Collectively, our findings identify PRMT5 as a prominent regulator of Tfh programming, with potential causal links to IL-2 signaling.
    Mesh-Begriff(e) Mice ; Animals ; Humans ; Interleukin-2/metabolism ; T-Lymphocytes, Helper-Inducer/metabolism ; T Follicular Helper Cells ; Influenza, Human ; Cell Differentiation ; Germinal Center ; Orthomyxoviridae ; Orthomyxoviridae Infections/metabolism
    Chemische Substanzen Interleukin-2
    Sprache Englisch
    Erscheinungsdatum 2024-03-04
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 3056-9
    ISSN 1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
    ISSN (online) 1550-6606
    ISSN 0022-1767 ; 1048-3233 ; 1047-7381
    DOI 10.4049/jimmunol.2300270
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Dysregulation of the TET family of epigenetic regulators in lymphoid and myeloid malignancies.

    Lio, Chan-Wang J / Yuita, Hiroshi / Rao, Anjana

    Blood

    2019  Band 134, Heft 18, Seite(n) 1487–1497

    Abstract: DNA methylation has pivotal regulatory roles in mammalian development, retrotransposon silencing, genomic imprinting, X-chromosome inactivation, and cancer. Cancer cells display highly dysregulated DNA methylation profiles, characterized by global ... ...

    Abstract DNA methylation has pivotal regulatory roles in mammalian development, retrotransposon silencing, genomic imprinting, X-chromosome inactivation, and cancer. Cancer cells display highly dysregulated DNA methylation profiles, characterized by global hypomethylation in conjunction with hypermethylation of promoter CpG islands; these changes are often correlated with promoter hypermethylation, leading to decreased expression of tumor suppressor genes, as well as with genome instability, leading to amplification and aberrant expression of oncogenes. Ten-eleven-translocation (TET) proteins are α-ketoglutarate (α-KG)-dependent dioxygenases that oxidize 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC) and the additional oxidation products 5-formylcytosine (5fC) and 5-carboxylcytosine (5caC); together, these oxidized methylcytosines are intermediates in DNA demethylation. TET2 is frequently mutated in diverse lymphoid and myeloid cancers, and TET loss of function is often observed in the absence of coding region mutations in TET genes. Despite our understanding of the biochemical activities of TET proteins, how TET loss of function promotes the onset and progression of hematopoietic malignancies is largely unknown. Here, we review recent advances in our understanding of the role of TET enzymes in lymphoid and myeloid neoplasms and highlight the importance of metabolic alterations that decrease TET activity in cancer initiation and progression.
    Mesh-Begriff(e) Animals ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/metabolism ; DNA Methylation/physiology ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Hematologic Neoplasms/enzymology ; Hematologic Neoplasms/genetics ; Humans ; Mutation
    Chemische Substanzen DNA-Binding Proteins
    Sprache Englisch
    Erscheinungsdatum 2019-08-30
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood.2019791475
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: Loss of TET2 and TET3 in regulatory T cells unleashes effector function

    Xiaojing Yue / Chan-Wang J. Lio / Daniela Samaniego-Castruita / Xiang Li / Anjana Rao

    Nature Communications, Vol 10, Iss 1, Pp 1-

    2019  Band 14

    Abstract: Loss of TET proteins in immune cell populations is known to result in immunopathology. Here the authors show that deficiency of Tet2 and Tet3 proteins, specifically in the CD4+ FoxP3+ Treg lineage, results in a dominant pathology in which ex-Treg cells ... ...

    Abstract Loss of TET proteins in immune cell populations is known to result in immunopathology. Here the authors show that deficiency of Tet2 and Tet3 proteins, specifically in the CD4+ FoxP3+ Treg lineage, results in a dominant pathology in which ex-Treg cells and bystander T cells gain aberrant effector function.
    Schlagwörter Science ; Q
    Sprache Englisch
    Erscheinungsdatum 2019-05-01T00:00:00Z
    Verlag Nature Publishing Group
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

    Volltext online

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  5. Artikel ; Online: Loss of TET2 and TET3 in regulatory T cells unleashes effector function

    Xiaojing Yue / Chan-Wang J. Lio / Daniela Samaniego-Castruita / Xiang Li / Anjana Rao

    Nature Communications, Vol 10, Iss 1, Pp 1-

    2019  Band 14

    Abstract: Loss of TET proteins in immune cell populations is known to result in immunopathology. Here the authors show that deficiency of Tet2 and Tet3 proteins, specifically in the CD4+ FoxP3+ Treg lineage, results in a dominant pathology in which ex-Treg cells ... ...

    Abstract Loss of TET proteins in immune cell populations is known to result in immunopathology. Here the authors show that deficiency of Tet2 and Tet3 proteins, specifically in the CD4+ FoxP3+ Treg lineage, results in a dominant pathology in which ex-Treg cells and bystander T cells gain aberrant effector function.
    Schlagwörter Science ; Q
    Sprache Englisch
    Erscheinungsdatum 2019-05-01T00:00:00Z
    Verlag Nature Portfolio
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  6. Artikel ; Online: The tumor suppressor kinase DAPK3 drives tumor-intrinsic immunity through the STING-IFN-β pathway.

    Takahashi, Mariko / Lio, Chan-Wang J / Campeau, Anaamika / Steger, Martin / Ay, Ferhat / Mann, Matthias / Gonzalez, David J / Jain, Mohit / Sharma, Sonia

    Nature immunology

    2021  Band 22, Heft 4, Seite(n) 485–496

    Abstract: Evasion of host immunity is a hallmark of cancer; however, mechanisms linking oncogenic mutations and immune escape are incompletely understood. Through loss-of-function screening of 1,001 tumor suppressor genes, we identified death-associated protein ... ...

    Abstract Evasion of host immunity is a hallmark of cancer; however, mechanisms linking oncogenic mutations and immune escape are incompletely understood. Through loss-of-function screening of 1,001 tumor suppressor genes, we identified death-associated protein kinase 3 (DAPK3) as a previously unrecognized driver of anti-tumor immunity through the stimulator of interferon genes (STING) pathway of cytosolic DNA sensing. Loss of DAPK3 expression or kinase activity impaired STING activation and interferon (IFN)-β-stimulated gene induction. DAPK3 deficiency in IFN-β-producing tumors drove rapid growth and reduced infiltration of CD103
    Mesh-Begriff(e) Animals ; Antineoplastic Combined Chemotherapy Protocols/pharmacology ; Cell Line, Tumor ; Death-Associated Protein Kinases/genetics ; Death-Associated Protein Kinases/metabolism ; Female ; Gene Expression Regulation, Neoplastic ; Human Umbilical Vein Endothelial Cells/enzymology ; Human Umbilical Vein Endothelial Cells/metabolism ; Humans ; Immune Checkpoint Inhibitors/pharmacology ; Immunity, Innate/drug effects ; Interferon-beta/genetics ; Interferon-beta/metabolism ; LIM Domain Proteins/genetics ; LIM Domain Proteins/metabolism ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Mice, Inbred C57BL ; Mice, Knockout ; Neoplasms/drug therapy ; Neoplasms/enzymology ; Neoplasms/genetics ; Neoplasms/immunology ; Phosphorylation ; Signal Transduction ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Tumor Escape/drug effects ; Ubiquitination ; Mice
    Chemische Substanzen Immune Checkpoint Inhibitors ; LIM Domain Proteins ; LMO7 protein, human ; Lmo7 protein, mouse ; Membrane Proteins ; STING1 protein, human ; Sting1 protein, mouse ; Transcription Factors ; Interferon-beta (77238-31-4) ; DAPK3 protein, human (EC 2.7.11.1) ; Dapk3 protein, mouse (EC 2.7.11.1) ; Death-Associated Protein Kinases (EC 2.7.11.1)
    Sprache Englisch
    Erscheinungsdatum 2021-03-25
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2016987-5
    ISSN 1529-2916 ; 1529-2908
    ISSN (online) 1529-2916
    ISSN 1529-2908
    DOI 10.1038/s41590-021-00896-3
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel ; Online: BATF and IRF4 cooperate to counter exhaustion in tumor-infiltrating CAR T cells.

    Seo, Hyungseok / González-Avalos, Edahí / Zhang, Wade / Ramchandani, Payal / Yang, Chao / Lio, Chan-Wang J / Rao, Anjana / Hogan, Patrick G

    Nature immunology

    2021  Band 22, Heft 8, Seite(n) 983–995

    Abstract: The transcription factors nuclear factor of activated T cells (NFAT) and activator protein 1 (AP-1; Fos-Jun) cooperate to promote the effector functions of T cells, but NFAT in the absence of AP-1 imposes a negative feedback program of T cell ... ...

    Abstract The transcription factors nuclear factor of activated T cells (NFAT) and activator protein 1 (AP-1; Fos-Jun) cooperate to promote the effector functions of T cells, but NFAT in the absence of AP-1 imposes a negative feedback program of T cell hyporesponsiveness (exhaustion). Here, we show that basic leucine zipper ATF-like transcription factor (BATF) and interferon regulatory factor 4 (IRF4) cooperate to counter T cell exhaustion in mouse tumor models. Overexpression of BATF in CD8
    Mesh-Begriff(e) Animals ; Basic-Leucine Zipper Transcription Factors/metabolism ; CD8-Positive T-Lymphocytes/immunology ; Cell Line, Tumor ; Disease Models, Animal ; Female ; Humans ; Interferon Regulatory Factors/metabolism ; Lymphocytes, Tumor-Infiltrating/immunology ; Male ; Melanoma, Experimental ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; NFATC Transcription Factors/metabolism ; Neoplasm Recurrence, Local/immunology ; Neoplasms/immunology ; Receptors, Chimeric Antigen/immunology ; Transcription Factor AP-1/metabolism
    Chemische Substanzen Basic-Leucine Zipper Transcription Factors ; Batf protein, mouse ; Interferon Regulatory Factors ; NFATC Transcription Factors ; Receptors, Chimeric Antigen ; Transcription Factor AP-1 ; interferon regulatory factor-4
    Sprache Englisch
    Erscheinungsdatum 2021-07-19
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2016987-5
    ISSN 1529-2916 ; 1529-2908
    ISSN (online) 1529-2916
    ISSN 1529-2908
    DOI 10.1038/s41590-021-00964-8
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  8. Artikel: TET methylcytosine oxidases: new insights from a decade of research

    Lio, Chan-Wang J / Yue, Xiaojing / López-Moyado, Isaac F / Tahiliani, Mamta / Aravind, L / Rao, Anjana

    Journal of biosciences. 2020 Dec., v. 45, no. 1

    2020  

    Abstract: In mammals, DNA methyltransferases transfer a methyl group from S-adenosylmethionine to the 5 position of cytosine in DNA. The product of this reaction, 5-methylcytosine (5mC), has many roles, particularly in suppressing transposable and repeat elements ... ...

    Abstract In mammals, DNA methyltransferases transfer a methyl group from S-adenosylmethionine to the 5 position of cytosine in DNA. The product of this reaction, 5-methylcytosine (5mC), has many roles, particularly in suppressing transposable and repeat elements in DNA. Moreover, in many cellular systems, cell lineage specification is accompanied by DNA demethylation at the promoters of genes expressed at high levels in the differentiated cells. However, since direct cleavage of the C-C bond connecting the methyl group to the 5 position of cytosine is thermodynamically disfavoured, the question of whether DNA methylation was reversible remained unclear for many decades. This puzzle was solved by our discovery of the TET (Ten-Eleven Translocation) family of 5-methylcytosine oxidases, which use reduced iron, molecular oxygen and the tricarboxylic acid cycle metabolite 2-oxoglutarate (also known as α-ketoglutarate) to oxidise the methyl group of 5mC to 5-hydroxymethylcytosine (5hmC) and beyond. TET-generated oxidised methylcytosines are intermediates in at least two pathways of DNA demethylation, which differ in their dependence on DNA replication. In the decade since their discovery, TET enzymes have been shown to have important roles in embryonic development, cell lineage specification, neuronal function and cancer. We review these findings and discuss their implications here.
    Schlagwörter DNA ; DNA demethylation ; DNA methylation ; DNA replication ; S-adenosylmethionine ; cells ; cytosine ; embryogenesis ; genes ; iron ; mammals ; metabolites ; methyltransferases ; neurons ; oxygen ; research ; thermodynamics ; tricarboxylic acid cycle
    Sprache Englisch
    Erscheinungsverlauf 2020-12
    Umfang p. 21.
    Erscheinungsort Springer India
    Dokumenttyp Artikel
    Anmerkung NAL-light
    ZDB-ID 756157-x
    ISSN 0973-7138 ; 0250-5991
    ISSN (online) 0973-7138
    ISSN 0250-5991
    DOI 10.1007/s12038-019-9973-4
    Datenquelle NAL Katalog (AGRICOLA)

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  9. Artikel ; Online: Loss of TET2 and TET3 in regulatory T cells unleashes effector function.

    Yue, Xiaojing / Lio, Chan-Wang J / Samaniego-Castruita, Daniela / Li, Xiang / Rao, Anjana

    Nature communications

    2019  Band 10, Heft 1, Seite(n) 2011

    Abstract: TET enzymes oxidize 5-methylcytosine to 5-hydroxymethylcytosine and other oxidized methylcytosines in DNA. Here we examine the role of TET proteins in regulatory T (Treg) cells. Tet2/ ... ...

    Abstract TET enzymes oxidize 5-methylcytosine to 5-hydroxymethylcytosine and other oxidized methylcytosines in DNA. Here we examine the role of TET proteins in regulatory T (Treg) cells. Tet2/3
    Mesh-Begriff(e) Adoptive Transfer ; Animals ; Bone Marrow Transplantation ; Colitis ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/immunology ; DNA-Binding Proteins/metabolism ; Dioxygenases ; Disease Models, Animal ; Female ; Humans ; Inflammation/genetics ; Inflammation/immunology ; Inflammation/pathology ; Male ; Mice ; Mice, Knockout ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/immunology ; Proto-Oncogene Proteins/metabolism ; T-Lymphocytes, Regulatory/immunology ; T-Lymphocytes, Regulatory/metabolism ; T-Lymphocytes, Regulatory/transplantation ; Transplantation Chimera
    Chemische Substanzen DNA-Binding Proteins ; Proto-Oncogene Proteins ; Dioxygenases (EC 1.13.11.-) ; Tet2 protein, mouse (EC 1.13.11.-) ; Tet3 protein, mouse (EC 1.13.11.-)
    Sprache Englisch
    Erscheinungsdatum 2019-05-01
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-019-09541-y
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  10. Artikel ; Online: Epigenetic remodeling by vitamin C potentiates plasma cell differentiation.

    Chen, Heng-Yi / Almonte-Loya, Ana / Lay, Fang-Yun / Hsu, Michael / Johnson, Eric / González-Avalos, Edahí / Yin, Jieyun / Bruno, Richard S / Ma, Qin / Ghoneim, Hazem E / Wozniak, Daniel J / Harrison, Fiona E / Lio, Chan-Wang Jerry

    eLife

    2022  Band 11

    Abstract: Ascorbate (vitamin C) is an essential micronutrient in humans. The severe chronic deficiency of ascorbate, termed scurvy, has long been associated with increased susceptibility to infections. How ascorbate affects the immune system at the cellular and ... ...

    Abstract Ascorbate (vitamin C) is an essential micronutrient in humans. The severe chronic deficiency of ascorbate, termed scurvy, has long been associated with increased susceptibility to infections. How ascorbate affects the immune system at the cellular and molecular levels remained unclear. From a micronutrient analysis, we identified ascorbate as a potent enhancer for antibody response by facilitating the IL-21/STAT3-dependent plasma cell differentiation in mouse and human B cells. The effect of ascorbate is unique as other antioxidants failed to promote plasma cell differentiation. Ascorbate is especially critical during early B cell activation by poising the cells to plasma cell lineage without affecting the proximal IL-21/STAT3 signaling and the overall transcriptome. As a cofactor for epigenetic enzymes, ascorbate facilitates TET2/3-mediated DNA modification and demethylation of multiple elements at the
    Mesh-Begriff(e) Animals ; Ascorbic Acid/pharmacology ; Cell Differentiation ; Epigenesis, Genetic ; Epigenomics ; Humans ; Mice ; Vitamins
    Chemische Substanzen Vitamins ; Ascorbic Acid (PQ6CK8PD0R)
    Sprache Englisch
    Erscheinungsdatum 2022-09-07
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2687154-3
    ISSN 2050-084X ; 2050-084X
    ISSN (online) 2050-084X
    ISSN 2050-084X
    DOI 10.7554/eLife.73754
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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