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Article ; Online: Immunity in the brain and surrounding tissues.

Kanamori, Mitsuhiro / Ito, Minako

2023 Volume 173, Issue 3, Page(s) 145–151

Abstract: Immune reactions in the brain, the most complex organ that directly or indirectly regulates almost every part of the body and its actions, need to be tightly regulated. Recent findings in the field of neuroimmunology have enhanced our understanding of ... ...

Abstract	Immune reactions in the brain, the most complex organ that directly or indirectly regulates almost every part of the body and its actions, need to be tightly regulated. Recent findings in the field of neuroimmunology have enhanced our understanding of immune cells not only inside the brain but also in adjacent tissues. Multiple types of immune cells exist and are active in neighboring border tissues, even in the steady state. In addition, advances in technology have allowed researchers to characterize a broad range of cell types, including stromal cells that support immune reactions. This review presents a short overview of the roles of the immune system in the brain during health and disease, with focus on adaptive immunity and anatomical sites of action. We also discuss potential roles of stromal cells.
MeSH term(s)	Brain ; Adaptive Immunity
Language	English
Publishing date	2023-02-01
Publishing country	England
Document type	Review ; Journal Article
ZDB-ID	218073-x
ISSN	1756-2651 ; 0021-924X
ISSN (online)	1756-2651
ISSN	0021-924X
DOI	10.1093/jb/mvad010
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Article: [Microglia and macrophages in diseases].

Kanamori, Mitsuhiro / Harada, Yoshihiro / Ito, Minako

Nihon yakurigaku zasshi. Folia pharmacologica Japonica

2023 Volume 158, Issue 4, Page(s) 304–307

Abstract: As the brain is a prime immune privileged organ, immune responses in it were not studied as intensively as other peripheral organs in the past. However, the brain is studded with immune cells called microglia, which play important roles particularly in ... ...

Abstract	As the brain is a prime immune privileged organ, immune responses in it were not studied as intensively as other peripheral organs in the past. However, the brain is studded with immune cells called microglia, which play important roles particularly in diseased conditions. In addition, from recent descriptive works, we have learned a lot about immune cells in neighboring tissues. Recent progress has rather made it clearer that the immune responses in and around the brain are complicated reactions with both positive and negative effects. And we still have not identified the way(s) we should pursue for clinical applications. Here we introduce microglia and macrophages in the steady state. We also discuss their roles in stroke, a major cause of death and disability in Japan, and Alzheimer's disease, which account for 60 to 70% of dementia.
MeSH term(s)	Humans ; Microglia ; Macrophages/physiology ; Brain ; Alzheimer Disease/etiology ; Stroke
Language	Japanese
Publishing date	2023-07-03
Publishing country	Japan
Document type	English Abstract ; Journal Article
ZDB-ID	1097532-9
ISSN	1347-8397 ; 0015-5691
ISSN (online)	1347-8397
ISSN	0015-5691
DOI	10.1254/fpj.22155
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Article ; Online: Meningeal lymphatics "drain" brain tumors.

Kanamori, Mitsuhiro / Kipnis, Jonathan

Cell research

2020 Volume 30, Issue 3, Page(s) 191–192

MeSH term(s)	Brain Neoplasms ; Humans ; Lymphatic Vessels ; Monitoring, Immunologic ; Vascular Endothelial Growth Factor C
Chemical Substances	Vascular Endothelial Growth Factor C
Language	English
Publishing date	2020-02-28
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/s41422-020-0286-9
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Zs.A 5283: Show issues

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Article: Increased neutrophils in inflammatory bowel disease accelerate the accumulation of amyloid plaques in the mouse model of Alzheimer's disease.

Kaneko, Ryusei / Matsui, Ako / Watanabe, Mahiro / Harada, Yoshihiro / Kanamori, Mitsuhiro / Awata, Natsumi / Kawazoe, Mio / Takao, Tomoaki / Kobayashi, Yutaro / Kikutake, Chie / Suyama, Mikita / Saito, Takashi / Saido, Takaomi C / Ito, Minako

Inflammation and regeneration

2023 Volume 43, Issue 1, Page(s) 20

Abstract: Background: Alzheimer's disease (AD) is one of the neurodegenerative diseases and characterized by the appearance and accumulation of amyloid-β (Aβ) aggregates and phosphorylated tau with aging. The aggregation of Aβ, which is the main component of ... ...

Abstract	Background: Alzheimer's disease (AD) is one of the neurodegenerative diseases and characterized by the appearance and accumulation of amyloid-β (Aβ) aggregates and phosphorylated tau with aging. The aggregation of Aβ, which is the main component of senile plaques, is closely associated with disease progression. App Methods: Wild-type and App Results: An increase in aggregated Aβ was observed in the brains of App Conclusion: These results suggest that neutrophils infiltrate the AD brain parenchyma when acute colitis occurs, and this infiltration is significantly related to disease progression. Therefore, we propose that neutrophil-targeted therapies could reduce Aβ accumulation observed in early AD and prevent the increased risk of AD due to colitis.
Language	English
Publishing date	2023-03-15
Publishing country	England
Document type	Journal Article
ZDB-ID	2051471-2
ISSN	1880-9693 ; 0389-4290
ISSN	1880-9693 ; 0389-4290
DOI	10.1186/s41232-023-00257-7
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Article ; Online: Reprogramming of Th1 cells into regulatory T cells through rewiring of the metabolic status.

Kanamori, Mitsuhiro / Nakatsukasa, Hiroko / Ito, Minako / Chikuma, Shunsuke / Yoshimura, Akihiko

International immunology

2018 Volume 30, Issue 8, Page(s) 357–373

Abstract: T helper type 1 (Th1) cells form one of the most stable CD4 T-cell subsets, and direct conversion of fully differentiated Th1 to regulatory T (Treg) cells has been poorly investigated. Here, we established a culture method for inducing Foxp3 from Th1 ... ...

Abstract	T helper type 1 (Th1) cells form one of the most stable CD4 T-cell subsets, and direct conversion of fully differentiated Th1 to regulatory T (Treg) cells has been poorly investigated. Here, we established a culture method for inducing Foxp3 from Th1 cells of mice and humans. This is achieved simply by resting Th1 cells without T-cell receptor ligation before stimulation in the presence of transforming growth factor-beta (TGF-β). We named the resulting Th1-derived Foxp3+ cells Th1reg cells. Mouse Th1reg cells showed an inducible Treg-like phenotype and suppressive ability both in vitro and in vivo. Th1reg cells could also be induced from in vivo-developed mouse Th1 cells. Unexpectedly, the resting process enabled Foxp3 expression not through epigenetic changes at the locus, but through metabolic change resulting from reduced mammalian target of rapamycin complex 1 (mTORC1) activity. mTORC1 suppressed TGF-β-induced phosphorylation of Smad2/3 in Th1 cells, which was restored in rested cells. Our study warrants future research aiming at development of immunotherapy with Th1reg cells.
MeSH term(s)	Adult ; Animals ; Cellular Reprogramming ; Humans ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; T-Lymphocytes, Regulatory/cytology ; T-Lymphocytes, Regulatory/immunology ; T-Lymphocytes, Regulatory/metabolism ; Th1 Cells/cytology ; Th1 Cells/immunology ; Th1 Cells/metabolism
Language	English
Publishing date	2018-06-27
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1013745-2
ISSN	1460-2377 ; 0953-8178
ISSN (online)	1460-2377
ISSN	0953-8178
DOI	10.1093/intimm/dxy043
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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: Stabilization of Foxp3 expression by CRISPR-dCas9-based epigenome editing in mouse primary T cells.

Okada, Masahiro / Kanamori, Mitsuhiro / Someya, Kazue / Nakatsukasa, Hiroko / Yoshimura, Akihiko

Epigenetics & chromatin

2017 Volume 10, Page(s) 24

Abstract: Background: Epigenome editing is expected to manipulate transcription and cell fates and to elucidate the gene expression mechanisms in various cell types. For functional epigenome editing, assessing the chromatin context-dependent activity of ... ...

Abstract	Background: Epigenome editing is expected to manipulate transcription and cell fates and to elucidate the gene expression mechanisms in various cell types. For functional epigenome editing, assessing the chromatin context-dependent activity of artificial epigenetic modifier is required. Results: In this study, we applied clustered regularly interspaced short palindromic repeats (CRISPR)-dCas9-based epigenome editing to mouse primary T cells, focusing on the Conclusions: Our results showed that artificial epigenome editing modified the epigenetic status and gene expression of the targeted loci, and engineered cellular functions in conjunction with endogenous epigenetic modification, suggesting effective usage of these technologies, which help elucidate the relationship between chromatin states and gene expression.
MeSH term(s)	Animals ; CRISPR-Cas Systems/genetics ; DNA Methylation/genetics ; DNA-Binding Proteins/genetics ; E1A-Associated p300 Protein/genetics ; Epigenomics ; Forkhead Transcription Factors/biosynthesis ; Forkhead Transcription Factors/genetics ; Gene Editing ; Gene Expression Regulation/genetics ; Mice ; Promoter Regions, Genetic ; Proto-Oncogene Proteins/genetics ; T-Lymphocytes, Regulatory/metabolism ; Transforming Growth Factor beta/genetics
Chemical Substances	DNA-Binding Proteins ; Forkhead Transcription Factors ; Foxp3 protein, mouse ; Proto-Oncogene Proteins ; TET1 protein, mouse ; Transforming Growth Factor beta ; E1A-Associated p300 Protein (EC 2.3.1.48) ; EP300 protein, human (EC 2.3.1.48)
Language	English
Publishing date	2017
Publishing country	England
Document type	Journal Article
ZDB-ID	2462129-8
ISSN	1756-8935 ; 1756-8935
ISSN (online)	1756-8935
ISSN	1756-8935
DOI	10.1186/s13072-017-0129-1
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Article ; Online: Suppressors of cytokine signaling: Potential immune checkpoint molecules for cancer immunotherapy.

Chikuma, Shunsuke / Kanamori, Mitsuhiro / Mise-Omata, Setsuko / Yoshimura, Akihiko

Cancer science

2017 Volume 108, Issue 4, Page(s) 574–580

Abstract: Inhibition of immune checkpoint molecules, PD-1 and CTLA4, has been shown to be a promising cancer treatment. PD-1 and CTLA4 inhibit TCR and co-stimulatory signals. The third T cell activation signal represents the signals from the cytokine receptors. ... ...

Abstract	Inhibition of immune checkpoint molecules, PD-1 and CTLA4, has been shown to be a promising cancer treatment. PD-1 and CTLA4 inhibit TCR and co-stimulatory signals. The third T cell activation signal represents the signals from the cytokine receptors. The cytokine interferon-γ (IFNγ) plays an important role in anti-tumor immunity by activating cytotoxic T cells (CTLs). Most cytokines use the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway, and the suppressors of cytokine signaling (SOCS) family of proteins are major negative regulators of the JAK/STAT pathway. Among SOCS proteins, CIS, SOCS1, and SOCS3 proteins can be considered the third immunocheckpoint molecules since they regulate cytokine signals that control the polarization of CD4
MeSH term(s)	Animals ; Humans ; Immunotherapy/methods ; Models, Immunological ; Neoplasms/immunology ; Neoplasms/metabolism ; Neoplasms/therapy ; Signal Transduction/immunology ; Suppressor of Cytokine Signaling 1 Protein/immunology ; Suppressor of Cytokine Signaling 1 Protein/metabolism ; Suppressor of Cytokine Signaling 3 Protein/immunology ; Suppressor of Cytokine Signaling 3 Protein/metabolism ; Suppressor of Cytokine Signaling Proteins/immunology ; Suppressor of Cytokine Signaling Proteins/metabolism ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism
Chemical Substances	Suppressor of Cytokine Signaling 1 Protein ; Suppressor of Cytokine Signaling 3 Protein ; Suppressor of Cytokine Signaling Proteins ; cytokine inducible SH2-containing protein
Language	English
Publishing date	2017-04-19
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.13194
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Article ; Online: Nr4a Receptors Regulate Development and Death of Labile Treg Precursors to Prevent Generation of Pathogenic Self-Reactive Cells.

Sekiya, Takashi / Hibino, Sana / Saeki, Keita / Kanamori, Mitsuhiro / Takaki, Satoshi / Yoshimura, Akihiko

Cell reports

2018 Volume 24, Issue 6, Page(s) 1627–1638.e6

Abstract: Regulatory T (Treg) cells develop from a self-reactive, CD4-single positive (CD4SP) precursor cell pool. Thus, Treg-fated developing thymocytes are expected to possess the potential to generate pathogenic self-reactive cells. However, no such pathogenic ... ...

Abstract	Regulatory T (Treg) cells develop from a self-reactive, CD4-single positive (CD4SP) precursor cell pool. Thus, Treg-fated developing thymocytes are expected to possess the potential to generate pathogenic self-reactive cells. However, no such pathogenic conversion has been observed, indicating mechanisms of defense to prevent such a deleterious event. Here, we show that, after the initial developmental phase, the Nr4a family of nuclear receptors promotes the development of Treg cells by cooperating with other Treg cell developmental machineries, as well as by forming a reinforcing loop with Foxp3. Nr4a-deficient Treg-fated thymocytes survive and can elicit autoimmunity, highlighting their roles in elimination of developing Treg precursors that fail to complete their development. Our findings reveal that the defective development of Treg-fated thymocytes is a potential route for the generation of pathogenic self-reactive cells, which is normally suppressed by Nr4a factors at both developmental and cell death levels.
MeSH term(s)	Animals ; Cell Differentiation ; Humans ; Mice ; Nuclear Receptor Subfamily 4, Group A, Member 1/metabolism ; T-Lymphocytes, Regulatory/immunology ; Transfection
Chemical Substances	NR4A1 protein, human ; Nuclear Receptor Subfamily 4, Group A, Member 1
Language	English
Publishing date	2018-08-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2018.07.008
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Article ; Online: Induced Regulatory T Cells: Their Development, Stability, and Applications.

Kanamori, Mitsuhiro / Nakatsukasa, Hiroko / Okada, Masahiro / Lu, Qianjin / Yoshimura, Akihiko

Trends in immunology

2016 Volume 37, Issue 11, Page(s) 803–811

Abstract: Regulatory T (Treg) cells, as central mediators of immune suppression, play crucial roles in many facets of immune systems. The transcription factor Foxp3 has been characterized as a master regulator of Tregs, and is induced during their thymic ... ...

Abstract	Regulatory T (Treg) cells, as central mediators of immune suppression, play crucial roles in many facets of immune systems. The transcription factor Foxp3 has been characterized as a master regulator of Tregs, and is induced during their thymic development. Foxp3
MeSH term(s)	Animals ; Cell Differentiation ; DNA Methylation ; Forkhead Transcription Factors/genetics ; Forkhead Transcription Factors/metabolism ; Humans ; Immunotherapy, Adoptive/methods ; Interleukin-2/metabolism ; Lymphocyte Activation ; T-Lymphocyte Subsets/physiology ; T-Lymphocytes, Regulatory/physiology ; T-Lymphocytes, Regulatory/transplantation ; Thymus Gland/immunology ; Transforming Growth Factor beta/metabolism
Chemical Substances	FOXP3 protein, human ; Forkhead Transcription Factors ; Interleukin-2 ; Transforming Growth Factor beta
Language	English
Publishing date	2016-11
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2036831-8
ISSN	1471-4981 ; 1471-4906
ISSN (online)	1471-4981
ISSN	1471-4906
DOI	10.1016/j.it.2016.08.012
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Zs.A 1601: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Role of scavenger receptors as damage-associated molecular pattern receptors in Toll-like receptor activation.

Komai, Kyoko / Shichita, Takashi / Ito, Minako / Kanamori, Mitsuhiro / Chikuma, Shunsuke / Yoshimura, Akihiko

International immunology

2017 Volume 29, Issue 2, Page(s) 59–70

Abstract: Damage-associated molecular patterns (DAMPs) have been implicated in sterile inflammation in various tissue injuries. High-mobility group box 1 (HMGB1) is a representative DAMP, and has been shown to transmit signals through receptors for advanced ... ...

Abstract	Damage-associated molecular patterns (DAMPs) have been implicated in sterile inflammation in various tissue injuries. High-mobility group box 1 (HMGB1) is a representative DAMP, and has been shown to transmit signals through receptors for advanced glycation end products (RAGEs) and TLRs, including TLR2 and TLR4. HMGB1 does not, however, bind to TLRs with high affinity; therefore, the mechanism of HMGB1-mediated TLR activation remains unclear. In this study, we found that fluorescently labeled HMGB1 was efficiently internalized into macrophages through class A scavenger receptors. Although both M1- and M2-type macrophages internalized HMGB1, only M1-type macrophages secreted cytokines in response to HMGB1. The pan-class A scavenger receptor competitive inhibitor, maleylated bovine serum albumin (M-BSA), inhibited HMGB1 internalization and reduced cytokine production from macrophages in response to HMGB1 but not to LPS. The C-terminal acidic domain of HMGB1 is responsible for scavenger receptor-mediated internalization and cytokine production. HMGB1 and TLR4 co-localized in macrophages, and this interaction was disrupted by M-BSA, suggesting that class A scavenger receptors function as co-receptors of HMGB1 for TLR activation. M-BSA ameliorated LPS-induced sepsis and dextran sulfate sodium (DSS)-induced colitis models in which HMGB1 has been shown to play progressive roles. These data suggest that scavenger receptors function as co-receptors along with TLRs for HMGB1 in M1-type inflammatory macrophages.
MeSH term(s)	Animals ; Cattle ; Cell Differentiation ; Cells, Cultured ; Colitis/chemically induced ; Colitis/immunology ; Cytokines/metabolism ; HMGB1 Protein/metabolism ; Humans ; Macrophages/physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Phenotype ; Receptors, Immunologic/genetics ; Receptors, Immunologic/metabolism ; Scavenger Receptors, Class A/genetics ; Scavenger Receptors, Class A/metabolism ; Sepsis/chemically induced ; Sepsis/immunology ; Serum Albumin, Bovine/administration & dosage ; Signal Transduction ; Toll-Like Receptor 2/genetics ; Toll-Like Receptor 2/metabolism ; Toll-Like Receptor 4/genetics ; Toll-Like Receptor 4/metabolism
Chemical Substances	Cytokines ; HMGB1 Protein ; HMGB1 protein, mouse ; Marco protein, mouse ; Msr1 protein, mouse ; Receptors, Immunologic ; Scavenger Receptors, Class A ; Tlr2 protein, mouse ; Tlr4 protein, mouse ; Toll-Like Receptor 2 ; Toll-Like Receptor 4 ; Serum Albumin, Bovine (27432CM55Q)
Language	English
Publishing date	2017-02-01
Publishing country	England
Document type	Journal Article
ZDB-ID	1013745-2
ISSN	1460-2377 ; 0953-8178
ISSN (online)	1460-2377
ISSN	0953-8178
DOI	10.1093/intimm/dxx010
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