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

Lio, Chan-Wang J / Rao, Anjana

2019 Volume 10, Page(s) 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 term(s)	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
Chemical Substances	Biomarkers ; DNA-Binding Proteins ; Enzymes ; Proto-Oncogene Proteins ; 5-hydroxymethylcytosine (1123-95-1) ; 5-Methylcytosine (6R795CQT4H)
Language	English
Publishing date	2019-02-12
Publishing country	Switzerland
Document type	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
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; 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 Volume 212, Issue 9, Page(s) 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 term(s)	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
Chemical Substances	Interleukin-2
Language	English
Publishing date	2024-02-16
Publishing country	United States
Document type	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
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Article ; Online: Dysregulation of the TET family of epigenetic regulators in lymphoid and myeloid malignancies.

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

Blood

2019 Volume 134, Issue 18, Page(s) 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 term(s)	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
Chemical Substances	DNA-Binding Proteins
Language	English
Publishing date	2019-08-30
Publishing country	United States
Document type	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
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Article ; 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 Volume 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.
Keywords	Science ; Q
Language	English
Publishing date	2019-05-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; 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 Volume 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 and bystander T cells gain aberrant effector function.
Keywords	Science ; Q
Language	English
Publishing date	2019-05-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; 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 Volume 22, Issue 4, Page(s) 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 term(s)	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
Chemical Substances	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)
Language	English
Publishing date	2021-03-25
Publishing country	United States
Document type	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
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Zs.A 5294: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 42: Show issues

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Article ; 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 Volume 22, Issue 8, Page(s) 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 term(s)	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
Chemical Substances	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
Language	English
Publishing date	2021-07-19
Publishing country	United States
Document type	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
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Zs.A 5294: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article: 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.
Keywords	DNA ; DNA demethylation ; DNA methylation ; DNA replication ; S-adenosylmethionine ; cells ; cytosine ; embryogenesis ; genes ; iron ; mammals ; metabolites ; methyltransferases ; neurons ; oxygen ; research ; thermodynamics ; tricarboxylic acid cycle
Language	English
Dates of publication	2020-12
Size	p. 21.
Publishing place	Springer India
Document type	Article
Note	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
Database	NAL-Catalogue (AGRICOLA)

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Article ; 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 Volume 10, Issue 1, Page(s) 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 term(s)	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
Chemical Substances	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.-)
Language	English
Publishing date	2019-05-01
Publishing country	England
Document type	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
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Article ; 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 Volume 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 term(s)	Animals ; Ascorbic Acid/pharmacology ; Cell Differentiation ; Epigenesis, Genetic ; Epigenomics ; Humans ; Mice ; Vitamins
Chemical Substances	Vitamins ; Ascorbic Acid (PQ6CK8PD0R)
Language	English
Publishing date	2022-09-07
Publishing country	England
Document type	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
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