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Article ; Online: Potential of HMGB-inhibitory oligodeoxynucleotide ISM ODN to neutrophil recruitment in mouse model of hepatitis.

Inoue, Asuka / Chiba, Shiho / Eto, Shotaro / Taniguchi, Tadatsugu / Yanai, Hideyuki

Genes to cells : devoted to molecular & cellular mechanisms

2022 Volume 28, Issue 3, Page(s) 202–210

Abstract: High-mobility group box 1 (HMGB1) is a nucleotide-binding chromatin protein that has also been characterized as a prototypical damage-associate molecular pattern. It triggers inflammatory responses upon release from damaged or dying cells. In fact, HMGB1 ...

Abstract	High-mobility group box 1 (HMGB1) is a nucleotide-binding chromatin protein that has also been characterized as a prototypical damage-associate molecular pattern. It triggers inflammatory responses upon release from damaged or dying cells. In fact, HMGB1 has been linked to the induction of many inflammatory diseases through immune cell activation including neutrophil recruitment. In this study, we examined the impact of HMGB1-binding inhibitory oligodeoxynucleotide (ISM ODN) on the development of hepatitis using a murine model of the disease. Our results indicate that ISM ODN effectively suppresses pathological features of hepatitis, including neutrophil accumulation. This study therefore may offer clinical insight into the treatment of hepatitis and possibly other inflammatory diseases.
MeSH term(s)	Mice ; Animals ; HMGB1 Protein/metabolism ; Oligodeoxyribonucleotides/pharmacology ; Disease Models, Animal ; Neutrophil Infiltration ; Hepatitis
Chemical Substances	HMGB1 Protein ; Oligodeoxyribonucleotides
Language	English
Publishing date	2022-12-27
Publishing country	England
Document type	Journal Article
ZDB-ID	1330000-3
ISSN	1365-2443 ; 1356-9597
ISSN (online)	1365-2443
ISSN	1356-9597
DOI	10.1111/gtc.13002
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Zs.A 4539: Show issues

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Article ; Online: Signal-transducing innate receptors in tumor immunity.

Hangai, Sho / Kimura, Yoshitaka / Taniguchi, Tadatsugu / Yanai, Hideyuki

Cancer science

2021 Volume 112, Issue 7, Page(s) 2578–2591

Abstract: The signal-transducing innate receptors represent classes of pattern recognition receptors (PRRs) that play crucial roles in the first line of the host defense against infections by the recognition of pathogen-derived molecules. Because of their poorly ... ...

Abstract	The signal-transducing innate receptors represent classes of pattern recognition receptors (PRRs) that play crucial roles in the first line of the host defense against infections by the recognition of pathogen-derived molecules. Because of their poorly discriminative nature compared with antigen receptors of the adaptive immune system, they also recognize endogenous molecules and evoke immune responses without infection, resulting in the regulation of tumor immunity. Therefore, PRRs may be promising targets for effective cancer immunotherapy, either by activating or inhibiting them. Here, we summarize our current knowledge of signal-transducing PRRs in the regulation of tumor immunity.
MeSH term(s)	Animals ; Cell Membrane/metabolism ; Cytoplasm/metabolism ; Humans ; Immunity, Innate ; Immunotherapy/trends ; Neoplasms/immunology ; Neoplasms/therapy ; Receptors, Pattern Recognition/immunology ; Receptors, Pattern Recognition/metabolism ; Signal Transduction/immunology ; Tumor Microenvironment/immunology
Chemical Substances	Receptors, Pattern Recognition
Language	English
Publishing date	2021-05-01
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2115647-5
ISSN	1349-7006 ; 1347-9032
ISSN (online)	1349-7006
ISSN	1347-9032
DOI	10.1111/cas.14848
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: [Regulation of innate immune responses by nucleic acid analogues].

Yanai, Hideyuki

Uirusu

2012 Volume 61, Issue 2, Page(s) 141–152

Abstract: The activation of innate immune responses by nucleic acids is critical to host responses against pathogens, such as viruses; however, nucleic acids can also trigger the development and/or exacerbation of pathogenic responses such as autoimmunity. We ... ...

Abstract	The activation of innate immune responses by nucleic acids is critical to host responses against pathogens, such as viruses; however, nucleic acids can also trigger the development and/or exacerbation of pathogenic responses such as autoimmunity. We previously demonstrated that the selective activation of nucleic acid-sensing cytosolic and Toll-like receptors is contingent on the promiscuous sensing of nucleic acids by high-mobility group box proteins (HMGBs). Basides these findings, we also found that nonimmunogenic nucleotide with high-affinity HMGB binding, termed ISM ODN, functions as suppressing agent for nucleic acid-activated innate immune responses. In this review, we aim to summerize this novel feature of HMGB proteins in nucleic acid-mediated innate immune responses. In addition, we will discuss the inhibitory effect of nonimmunogenic oligodeoxynucleotides (ni-ODNs) targeting HMGB proteins.
MeSH term(s)	Autoimmune Diseases/immunology ; HMGB Proteins/physiology ; Humans ; Immunity, Innate/immunology ; Immunomodulation ; Nucleic Acids/physiology ; Oligodeoxyribonucleotides/immunology ; Receptors, Pattern Recognition/physiology ; Signal Transduction/physiology ; Toll-Like Receptors/physiology
Chemical Substances	HMGB Proteins ; Nucleic Acids ; Oligodeoxyribonucleotides ; Receptors, Pattern Recognition ; Toll-Like Receptors
Language	Japanese
Publishing date	2012-07-15
Publishing country	Japan
Document type	English Abstract ; Journal Article ; Review
ZDB-ID	603272-2
ISSN	0042-6857
ISSN	0042-6857
DOI	10.2222/jsv.61.141
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Article ; Online: Damage-associated molecular patterns and Toll-like receptors in the tumor immune microenvironment.

Yanai, Hideyuki / Hangai, Sho / Taniguchi, Tadatsugu

International immunology

2020 Volume 33, Issue 12, Page(s) 841–846

Abstract: As clinically demonstrated by the success of immunotherapies to improve survival outcomes, tumors are known to gain a survival advantage by circumventing immune surveillance. A defining feature of this is the creation and maintenance of a tumor immune ... ...

Abstract	As clinically demonstrated by the success of immunotherapies to improve survival outcomes, tumors are known to gain a survival advantage by circumventing immune surveillance. A defining feature of this is the creation and maintenance of a tumor immune microenvironment (TIME) that directly and indirectly alters the host's immunologic signaling pathways through a variety of mechanisms. Tumor-intrinsic mechanisms that instruct the formation and maintenance of the TIME have been an area of intensive study, such as the identification and characterization of soluble factors actively and passively released by tumor cells that modulate immune cell function. In particular, damage-associated molecular pattern (DAMP) molecules typically released by necrotic tumor cells are recognized by innate immune receptors such as Toll-like receptors (TLRs) and stimulate immune cells within TIME. Given their broad and potent effects on the immune system, a better understanding for how DAMP and TLR interactions sculpt the TIME to favor tumor growth would identify new strategies and approaches for cancer immunotherapy.
MeSH term(s)	Animals ; Humans ; Neoplasms/immunology ; Toll-Like Receptors/immunology ; Tumor Microenvironment/immunology
Chemical Substances	Toll-Like Receptors
Language	English
Publishing date	2020-09-29
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1013745-2
ISSN	1460-2377 ; 0953-8178
ISSN (online)	1460-2377
ISSN	0953-8178
DOI	10.1093/intimm/dxab050
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Zs.A 2619: 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 ; Online: Tumor cell-derived spermidine is an oncometabolite that suppresses TCR clustering for intratumoral CD8

Hibino, Sana / Eto, Shotaro / Hangai, Sho / Endo, Keiko / Ashitani, Sanae / Sugaya, Maki / Osawa, Tsuyoshi / Soga, Tomoyoshi / Taniguchi, Tadatsugu / Yanai, Hideyuki

Proceedings of the National Academy of Sciences of the United States of America

2023 Volume 120, Issue 24, Page(s) e2305245120

Abstract: The activation and expansion of T cells that recognize cancer cells is an essential aspect to antitumor immunity. Tumors may escape destruction by the immune system through ectopic expression of inhibitory immune ligands typically exemplified by the PD- ... ...

Abstract	The activation and expansion of T cells that recognize cancer cells is an essential aspect to antitumor immunity. Tumors may escape destruction by the immune system through ectopic expression of inhibitory immune ligands typically exemplified by the PD-L1/PD-1 pathway. Here, we reveal another facet of tumor evasion from T cell surveillance. By secretome profiling of necrotic tumor cells, we identified an oncometabolite spermidine as a unique inhibitor of T cell receptor (TCR) signaling. Mechanistically, spermidine causes the downregulation of the plasma membrane cholesterol levels, resulting in the suppression of TCR clustering. Using syngeneic mouse models, we show that spermidine is abundantly detected in the tumor immune microenvironment (TIME) and that administration of the polyamine synthesis inhibitor effectively enhanced CD8
MeSH term(s)	Animals ; Mice ; Spermidine/pharmacology ; Spermidine/metabolism ; CD8-Positive T-Lymphocytes ; Neoplasms/metabolism ; Antineoplastic Agents/pharmacology ; Immunotherapy/methods ; Receptors, Antigen, T-Cell/metabolism ; Tumor Microenvironment ; Cell Line, Tumor ; B7-H1 Antigen/metabolism
Chemical Substances	Spermidine (U87FK77H25) ; Antineoplastic Agents ; Receptors, Antigen, T-Cell ; B7-H1 Antigen
Language	English
Publishing date	2023-06-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2305245120
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Zs.A 1148: Show issues

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Article ; Online: Fine-tuning type I IFN signaling: A new chapter in the IFN saga.

Yanai, Hideyuki / Taniguchi, Tadatsugu

Cell research

2017 Volume 27, Issue 12, Page(s) 1407–1408

Abstract: Type I interferon (IFN) signaling is critical for intracellular antimicrobial programmes, affecting both innate and adaptive immune responses. The paper recently published in Cell demonstrates a new regulatory mechanism of the type I IFN signaling ... ...

Abstract	Type I interferon (IFN) signaling is critical for intracellular antimicrobial programmes, affecting both innate and adaptive immune responses. The paper recently published in Cell demonstrates a new regulatory mechanism of the type I IFN signaling pathway by histone-lysine N-methyltransferase SETD2.
MeSH term(s)	Antiviral Agents ; Histone-Lysine N-Methyltransferase ; Interferon Type I ; Methylation ; Signal Transduction
Chemical Substances	Antiviral Agents ; Interferon Type I ; Histone-Lysine N-Methyltransferase (EC 2.1.1.43)
Language	English
Publishing date	2017-09-19
Publishing country	England
Document type	Journal Article ; Comment
ZDB-ID	1319303-x
ISSN	1748-7838 ; 1001-0602
ISSN (online)	1748-7838
ISSN	1001-0602
DOI	10.1038/cr.2017.118
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Zs.A 5283: Show issues

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Article ; Online: The impact of damage-associated molecules released from canine tumor cells on gene expression in macrophages.

Eto, Shotaro / Yanai, Hideyuki / Hangai, Sho / Kato, Daiki / Nishimura, Ryohei / Nakagawa, Takayuki

Scientific reports

2021 Volume 11, Issue 1, Page(s) 8525

Abstract: Dying or damaged cells that are not completely eradicated by the immune system release their intracellular components in the extracellular space. Aberrant exposure of the damage-associated molecules to the immune system is often associated with ... ...

Abstract	Dying or damaged cells that are not completely eradicated by the immune system release their intracellular components in the extracellular space. Aberrant exposure of the damage-associated molecules to the immune system is often associated with inflammation and cancer pathogenesis. Thus, elucidating the role of damage-associated molecules in inducing sterile immune responses is crucial. In this study, we show that prostaglandin E2 (PGE2) is produced in the supernatants from several types of canine necrotic tumor cell lines. Inhibition of PGE2 production by indomethacin, a potent inhibitor of cyclooxygenase (COX) enzymes, induces the expression of tumor necrosis factor (Tnf) mRNA in the necrotic tumor cell supernatants. These results comply with the previous observations reported in mouse cell lines. Furthermore, comprehensive ribonucleic acid-sequencing (RNA-seq) analysis revealed that three categories of genes were induced by the damage-associated molecules: (i) a group of PGE2-inducible genes, (ii) genes that promote inflammation and are suppressed by PGE2, and (iii) a group of genes not suppressed by PGE2. Collectively, our findings reveal the hitherto unknown immune regulatory system by PGE2 and damage-associated molecules, which may have clinical implications in inflammation and cancer.
MeSH term(s)	Animals ; Cell Line ; Cell Line, Tumor ; Cyclooxygenase 2/metabolism ; Dinoprostone/metabolism ; Dogs ; Gene Expression/genetics ; Inflammation/metabolism ; Macrophages/metabolism ; Mice ; RAW 264.7 Cells ; RNA, Messenger/metabolism ; Tumor Necrosis Factor-alpha/metabolism
Chemical Substances	RNA, Messenger ; Tumor Necrosis Factor-alpha ; Cyclooxygenase 2 (EC 1.14.99.1) ; Dinoprostone (K7Q1JQR04M)
Language	English
Publishing date	2021-04-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-87979-1
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: The Interferon (IFN) Class of Cytokines and the IFN Regulatory Factor (IRF) Transcription Factor Family.

Negishi, Hideo / Taniguchi, Tadatsugu / Yanai, Hideyuki

Cold Spring Harbor perspectives in biology

2018 Volume 10, Issue 11

Abstract: Interferons (IFNs) are a broad class of cytokines elicited on challenge to the host defense and are essential for mobilizing immune responses to pathogens. Divided into three classes, type I, type II, and type III, all IFNs share in common the ability to ...

Abstract	Interferons (IFNs) are a broad class of cytokines elicited on challenge to the host defense and are essential for mobilizing immune responses to pathogens. Divided into three classes, type I, type II, and type III, all IFNs share in common the ability to evoke antiviral activities initiated by the interaction with their cognate receptors. The nine-member IFN regulatory factor (IRF) family, first discovered in the context of transcriptional regulation of type I IFN genes following viral infection, are pivotal for the regulation of the IFN responses. In this review, we briefly describe cardinal features of the three types of IFNs and then focus on the role of the IRF family members in the regulation of each IFN system.
MeSH term(s)	Animals ; DNA ; Gene Expression Regulation/physiology ; Humans ; Interferon Regulatory Factors/genetics ; Interferon Regulatory Factors/metabolism ; Interferons/genetics ; Interferons/metabolism
Chemical Substances	Interferon Regulatory Factors ; DNA (9007-49-2) ; Interferons (9008-11-1)
Language	English
Publishing date	2018-11-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ISSN	1943-0264
ISSN (online)	1943-0264
DOI	10.1101/cshperspect.a028423
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: The impact of damage-associated molecules released from canine tumor cells on gene expression in macrophages

Shotaro Eto / Hideyuki Yanai / Sho Hangai / Daiki Kato / Ryohei Nishimura / Takayuki Nakagawa

Scientific Reports, Vol 11, Iss 1, Pp 1-

2021 Volume 13

Abstract: Abstract Dying or damaged cells that are not completely eradicated by the immune system release their intracellular components in the extracellular space. Aberrant exposure of the damage-associated molecules to the immune system is often associated with ... ...

Abstract	Abstract Dying or damaged cells that are not completely eradicated by the immune system release their intracellular components in the extracellular space. Aberrant exposure of the damage-associated molecules to the immune system is often associated with inflammation and cancer pathogenesis. Thus, elucidating the role of damage-associated molecules in inducing sterile immune responses is crucial. In this study, we show that prostaglandin E2 (PGE2) is produced in the supernatants from several types of canine necrotic tumor cell lines. Inhibition of PGE2 production by indomethacin, a potent inhibitor of cyclooxygenase (COX) enzymes, induces the expression of tumor necrosis factor (Tnf) mRNA in the necrotic tumor cell supernatants. These results comply with the previous observations reported in mouse cell lines. Furthermore, comprehensive ribonucleic acid-sequencing (RNA-seq) analysis revealed that three categories of genes were induced by the damage-associated molecules: (i) a group of PGE2-inducible genes, (ii) genes that promote inflammation and are suppressed by PGE2, and (iii) a group of genes not suppressed by PGE2. Collectively, our findings reveal the hitherto unknown immune regulatory system by PGE2 and damage-associated molecules, which may have clinical implications in inflammation and cancer.
Keywords	Medicine ; R ; Science ; Q
Subject code	616
Language	English
Publishing date	2021-04-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Acidic extracellular pH drives accumulation of N1-acetylspermidine and recruitment of protumor neutrophils.

Kato, Miki / Maeda, Keisuke / Nakahara, Ryuichi / Hirose, Haruka / Kondo, Ayano / Aki, Sho / Sugaya, Maki / Hibino, Sana / Nishida, Miyuki / Hasegawa, Manami / Morita, Hinano / Ando, Ritsuko / Tsuchida, Rika / Yoshida, Minoru / Kodama, Tatsuhiko / Yanai, Hideyuki / Shimamura, Teppei / Osawa, Tsuyoshi

PNAS nexus

2023 Volume 2, Issue 10, Page(s) pgad306

Abstract: An acidic tumor microenvironment plays a critical role in tumor progression. However, understanding of metabolic reprogramming of tumors in response to acidic extracellular pH has remained elusive. Using comprehensive metabolomic analyses, we ... ...

Abstract	An acidic tumor microenvironment plays a critical role in tumor progression. However, understanding of metabolic reprogramming of tumors in response to acidic extracellular pH has remained elusive. Using comprehensive metabolomic analyses, we demonstrated that acidic extracellular pH (pH 6.8) leads to the accumulation of N1-acetylspermidine, a protumor metabolite, through up-regulation of the expression of spermidine/spermine acetyltransferase 1 (
Language	English
Publishing date	2023-10-10
Publishing country	England
Document type	Journal Article
ISSN	2752-6542
ISSN (online)	2752-6542
DOI	10.1093/pnasnexus/pgad306
Database	MEDical Literature Analysis and Retrieval System OnLINE

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