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松本穣

徳島大学

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2024年4月30日更新

職名: 講師
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電子メール: m.matsumoto@tokushima-u.ac.jp
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学位: 医学博士 (徳島大学) (2020年6月)
職歴・経歴: 2018/9: 徳島大学助教, 大学院医歯薬学研究部 (-2021.7.)
2021/8: 徳島大学講師, 大学院医歯薬学研究部

専門分野・研究分野: 研究者総覧に該当データはありませんでした。

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2024年4月30日更新

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担当経験のある授業科目: ヒューマンサイエンス(病理病態学) (大学院)
病理学(Ⅰ・Ⅱ) (学部)
病理学Ⅰ・病理学Ⅰ実習 (学部)
病理学Ⅱ・病理学Ⅱ実習 (学部)
病理学実習 (学部)
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2024年4月30日更新

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著書

Yoshida Hideyuki, Mitsuru Matsumoto and Minoru Matsumoto :
Transcriptomics to Dissect the Immune System,
Springer, Mar. 2022.

(出版サイトへのリンク): ● Publication site (DOI): 10.1007/978-3-030-87821-4_10
(文献検索サイトへのリンク): ● Summary page in Scopus @ Elsevier: 2-s2.0-85153431635

(DOI: 10.1007/978-3-030-87821-4_10, Elsevier: Scopus) 森本純子, 宮澤龍一郎, 松本穣, 松本満 :
胸腺上皮細胞を対象とする自己免疫疾患への橋渡し研究の可能性,
北隆館 Precision Medicine 第3巻第12号, 東京, 2020年10月. 森本純子, 宮澤龍一郎, 松本穣, 松本満 :
自己免疫疾患(別冊 BIO Clinica 慢性炎症と疾患通巻24号第9巻第1巻), --- Aireを基軸とする自己免疫疾患の病態解明 ---,
北隆館, 東京, 2020年7月. Minoru Matsumoto, Rodrigues M. Pedro, Sousa Laura, Koichi Tsuneyama, Mitsuru Matsumoto and Alves L. Nuno :
The Ins and Outs of Thymic Epithelial Cell Differentiation and Function,
Springer, Apr. 2019.

論文

Minoru Matsumoto, 吉田英行, Koichi Tsuneyama, Takeshi Oya and Mitsuru Matsumoto :
Revisiting Aire and tissue-restricted antigens at single-cell resolution,
Frontiers in Immunology, Vol.14, 1176450, 2023. Junko Morimoto, Minoru Matsumoto, Takeshi Oya, Koichi Tsuneyama and Mitsuru Matsumoto :
Cooperative but Distinct Role of Medullary Thymic Epithelial Cells and Dendritic Cells in the Production of Regulatory T Cells in the Thymus.,
The Journal of Immunology, 2023.

(要約): Regulatory T cells (Tregs) are produced in the thymus to establish self-tolerance, and agonistic stimuli by self-Ags play a pivotal role in this process. Although two types of APCs, medullary thymic epithelial cells (mTECs) and dendritic cells (DCs), are responsible for presenting self-Ags together with costimulatory/cytokine signals, the distinct role of each APC in producing Tregs remains enigmatic. We have approached this issue by depleting the mTECs and DCs using mice expressing diphtheria toxin receptors driven by Aire and CD11c promoters, respectively. Depletion of mTECs showed an effect on Treg production quantitatively and qualitatively more profound than that of DCs followed by the development of distinct organ-specific autoimmune lesions in the hosts. Because self-Ags produced by mTECs are transferable to DCs through a process known as Ag transfer, we monitored the process of Ag transfer using mice expressing GFP from TECs. Although GFP expressed from total TECs was effectively transferred to DCs, GFP expressed from cortical TECs was not, suggesting that mTECs are the predominant source of self-Ags. We also found that GFP expressed not only from mature mTECs but also from immature mTECs was transferred to DCs, suggesting that a broad spectrum of molecules were subjected to Ag transfer during mTEC development. Interestingly, the numbers of recirculating non-Tregs producing IL-2, an important source for Treg expansion in the thymus, were reduced only in the mTEC-depleted mice. These results suggested the cooperative but distinct role of mTECs and DCs in the production of Tregs to avoid autoimmunity.
(出版サイトへのリンク): ● Publication site (DOI): 10.4049/jimmunol.2200780
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37067332; ● Search Scopus @ Elsevier (PMID): 37067332; ● Search Scopus @ Elsevier (DOI): 10.4049/jimmunol.2200780

(DOI: 10.4049/jimmunol.2200780, PubMed: 37067332) Minoru Matsumoto, Takuya Ohmura, Yuto Hanibuchi, Mayuko Shimizu, Yasuyo Saijo, Hirohisa Ogawa, Ryuichiro Miyazawa, Junko Morimoto, Koichi Tsuneyama, Mitsuru Matsumoto and Takeshi Oya :
AIRE illuminates the feature of medullary thymic epithelial cells in thymic carcinoma.,
Cancer Medicine, 2023.

(要約): Despite the clear distinction between cortical (cTECs) and medullary thymic epithelial cells (mTECs) in physiology, the cell of origin of thymic carcinomas (TCs) and other thymic epithelial tumors remained enigmatic. We addressed this issue by focusing on AIRE, an mTEC-specific transcriptional regulator that is required for immunological self-tolerance. We found that a large proportion of TCs expressed AIRE with typical nuclear dot morphology by immunohistochemistry. AIRE expression in TCs was supported by the RNA-seq data in the TCGA-THYM database. Furthermore, our bioinformatics approach to the recent single-cell RNA-seq data on human thymi has revealed that TCs hold molecular characteristics of multiple mTEC subpopulations. In contrast, TCs lacked the gene signatures for cTECs. We propose that TCs are tumors derived from mTECs.
(出版サイトへのリンク): ● Publication site (DOI): 10.1002/cam4.5777
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36912123; ● Search Scopus @ Elsevier (PMID): 36912123; ● Search Scopus @ Elsevier (DOI): 10.1002/cam4.5777

(DOI: 10.1002/cam4.5777, PubMed: 36912123) Ryuichiro Miyazawa, Jun-Ichi Nagao, Ken-Ichi Arita-Morioka, Minoru Matsumoto, Junko Morimoto, Yoshida Masaki, Takeshi Oya, Koichi Tsuneyama, Hedeyuki Yoshida, Yoshihiko Tanaka and Mitsuru Matsumoto :
Dispensable Role of Aire in CD11c+ Conventional Dendritic Cells for Antigen Presentation and Shaping the Transcriptome.,
ImmunoHorizons, Vol.7, No.1, 140-158, 2023.

(要約): Aire, the defect of which is responsible for the development of autoimmunity, is predominantly expressed in medullary thymic epithelial cells, and it controls a wide variety of genes, including those of tissue-restricted Ags, for establishing thymic tolerance. Aire is also expressed from APCs in the periphery, called extrathymic Aire-expressing cells (eTACs), and their complementing role to thymic tolerance has been suggested. eTACs are composed of two distinct classes of APCs, conventional dendritic cell (cDC)-type and group 3 innate lymphoid cell (ILC3)-like-type expressing retinoic acid receptor-related orphan receptor γt (RORγt). Although the essential role of Aire in the latter in the Th17-mediated immune response against Candida albicans has been reported, the role of Aire in the cDC-type eTACs for this action has not been examined. Furthermore, the significance of Aire in the production of the transcriptome of the cDC-type eTACs remains unknown. We have approached these issues using a high-fidelity Aire-reporter mouse strain. We found that although the cDC-type eTACs dominated ILC3-like-type eTACs in number and they served as efficient APCs for the immune response against an exogenous Ag as well as for the C. albicans-specific Th17 immune response, loss of Aire in cDC-type eTACs showed no clear effect on these functions. Furthermore, loss of Aire showed no major impact on the transcriptome from cDC-type eTACs. These results suggested that Aire in cDC-type eTACs may not have a cell-intrinsic role in the immune response in contrast to the role of Aire in ILC3-like-type eTACs.
(徳島大学機関リポジトリ): ● Metadata: 118793
(出版サイトへのリンク): ● Publication site (DOI): 10.4049/immunohorizons.2200103
(文献検索サイトへのリンク): ● Search Scopus @ Elsevier (DOI): 10.4049/immunohorizons.2200103

(徳島大学機関リポジトリ: 118793, DOI: 10.4049/immunohorizons.2200103) Satoshi Sumida, Mayuko Shimizu, Yuko Miyakami, Takumi Kakimoto, Tomoko Kobayashi, Yasuyo Saijo, Minoru Matsumoto, Hirohisa Ogawa, Takeshi Oya, Yoshimi Bando, Hisanori Uehara, Shu Taira, Mitsuo Shimada and Koichi Tsuneyama :
Histological and immunohistochemical analysis of epithelial cells in epidermoid cysts in intrapancreatic accessory spleen.,
The Journal of Medical Investigation : JMI, Vol.70, No.1.2, 251-259, 2023.

(要約): Novel histological features of epithelial cells of ECIPAS were indicated. Although more cases need to be evaluated, we propose that the cause of ECIPAS may be different from that of pancreatic ductal origin. J. Med. Invest. 70 : 251-259, February, 2023.
(キーワード): Humans / Epidermal Cyst / Spleen / Pancreatic Diseases / Epithelial Cells / Immunohistochemistry
(徳島大学機関リポジトリ): ● Metadata: 118205
(出版サイトへのリンク): ● Publication site (DOI): 10.2152/jmi.70.251
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37164730; ● Search Scopus @ Elsevier (PMID): 37164730; ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.70.251

(徳島大学機関リポジトリ: 118205, DOI: 10.2152/jmi.70.251, PubMed: 37164730) Hitoshi Nishijima, Mizuki Sugita, Natsuka Umezawa, Naoki Kimura, Hirokazu Sasaki, Hiroshi Kawano, Yasuhiko Nishioka, Minoru Matsumoto, Takeshi Oya, Koichi Tsuneyama, Junko Morimoto and Mitsuru Matsumoto :
Development of organ-specific autoimmunity by dysregulated Aire expression.,
Immunology and Cell Biology, Vol.100, No.5, 371-377, 2022.

(要約): Deficiency for AIRE/Aire in both humans and mice results in the development of organ-specific autoimmune disease. We tested whether augmented and/or dysregulated AIRE/Aire expression might be also prone to the breakdown of self-tolerance. To define the effect of augmented Aire expression on the development of autoimmunity, antigen-specific clonal deletion and production of clonotypic regulatory T cells (Tregs) in the thymus were examined using mice expressing two additional copies of Aire in a heterozygous state (3xAire-knockin mice: 3xAire-KI). We found that both clonal deletion of autoreactive T cells and production of clonotypic Tregs in the thymus from 3xAire-KI were impaired in a T-cell receptor-transgenic system. Furthermore, 3xAire-KI females showed higher scores of experimental autoimmune encephalomyelitis induced by myelin oligodendrocyte glycoprotein than wild-type littermates, suggesting that augmented Aire expression exacerbates organ-specific autoimmunity under disease-prone conditions. In humans, we found that one patient with amyopathic dermatomyositis showed CD3
(キーワード): Animals / 自己免疫 (autoimmunity) / Clonal Deletion / Encephalomyelitis, Autoimmune, Experimental / 女性 (female) / Humans / Immune Tolerance / Mice / Myelin-Oligodendrocyte Glycoprotein / Thymus Gland
(徳島大学機関リポジトリ): ● Metadata: 117817
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/imcb.12546
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35313042; ● Search Scopus @ Elsevier (PMID): 35313042; ● Search Scopus @ Elsevier (DOI): 10.1111/imcb.12546

(徳島大学機関リポジトリ: 117817, DOI: 10.1111/imcb.12546, PubMed: 35313042) Mayuko Shimizu, Soichiroh Ishimaru, Wai Yee Yan Christine, Takeo Minamikawa, Takaaki Tsunematsu, Aiko Endoh, Takumi Kojima, Minoru Matsumoto, Tomoko Kobayashi, Satoshi Sumida, Takumi Kakimoto, MIYAGAMI Yuko, Hirohisa Ogawa, Takeshi Oya and Koichi Tsuneyama :
Establishment of an epicutaneously sensitized murine model of shellfish allergy and evaluation of skin condition by Raman microscopy.,
Applied Sciences, Vol.12, No.3566, 2022.

(徳島大学機関リポジトリ): ● Metadata: 117211
(出版サイトへのリンク): ● Publication site (DOI): 10.3390/app12073566
(文献検索サイトへのリンク): ● Search Scopus @ Elsevier (DOI): 10.3390/app12073566

(徳島大学機関リポジトリ: 117211, DOI: 10.3390/app12073566) Junko Morimoto, Minoru Matsumoto, Ryuichiro Miyazawa, Takeshi Oya, Koichi Tsuneyama and Mitsuru Matsumoto :
No Major Impact of Two Homologous Proteins Ly6C1 and Ly6C2 on Immune Homeostasis.,
ImmunoHorizons, Vol.6, No.3, 202-210, 2022.

(要約): Ly6C comprises two homologous components of Ly6C1 and Ly6C2, and the expression of either of the Ly6C molecules defines unique functional subsets of monocytes. Ly6C is also expressed by other immune cell types, including Aire-expressing medullary thymic epithelial cells. Because the role of Ly6C expression in determining the functional subsets remains unclear, we generated mice deficient for both Ly6C1 and Ly6C2 with CRISPR-Cas9mediated deletion. Mice deficient for Ly6C1/Ly6C2 showed no major alterations in the subsets and function of monocyte and other immune cells, including the cells involved in the dextran sulfate sodium saltinduced colitis model. By generating the mice deficient for Ly6C1 alone, we have also investigated the expression pattern of Ly6C1 and Ly6C2 in immune cells. Except for medullary thymic epithelial cells and CD4 single-positive T cells, immune cells predominantly expressed Ly6C2. Thus, despite the importance as a marker with a unique differential expression pattern, the Ly6C molecules have no major impact on determining the functional subsets and maintaining immune homeostasis.
(徳島大学機関リポジトリ): ● Metadata: 117315
(出版サイトへのリンク): ● Publication site (DOI): 10.4049/immunohorizons.2100114
(文献検索サイトへのリンク): ● Search Scopus @ Elsevier (DOI): 10.4049/immunohorizons.2100114

(徳島大学機関リポジトリ: 117315, DOI: 10.4049/immunohorizons.2100114) Junko Morimoto, Minoru Matsumoto, Ryuichiro Miyazawa, Hideyuki Yoshida, Koichi Tsuneyama and Mitsuru Matsumoto :
Aire suppresses CTLA-4 expression from the thymic stroma to control autoimmunity.,
Cell Reports, Vol.38, No.7, 110384, 2022.

(要約): Impaired production of thymic regulatory T cells (Tregs) is implicated in the development of Aire-dependent autoimmunity. Because Tregs require agonistic T cell receptor stimuli by self-antigens to develop, reduced expression of self-antigens from medullary thymic epithelial cells (mTECs) has been considered to play a major role in the reduced Treg production in Aire deficiency. Here, we show that mTECs abnormally express co-inhibitory receptor CTLA-4 if Aire is non-functional. Upon binding with CD80/CD86 ligands expressed on thymic dendritic cells (DCs), the ectopically expressed CTLA-4 from Aire-deficient mTECs removes the CD80/CD86 ligands from the DCs. This attenuates the ability of DCs to provide co-stimulatory signals and to present self-antigens transferred from mTECs, both of which are required for Treg production. Accordingly, impaired production of Tregs and organ-specific autoimmunity in Aire-deficient mice are rescued by the depletion of CTLA-4 expression from mTECs. Our studies illuminate the significance of mTEC-DC interaction coordinated by Aire for the establishment of thymic tolerance.
(キーワード): Animals / Antigens, CD / Autoantigens / Autoimmunity / CTLA-4 Antigen / Epithelial Cells / Ligands / Mice, Inbred BALB C / Mice, Inbred C57BL / Organ Specificity / Stromal Cells / T-Lymphocytes, Regulatory / Thymus Gland / Transcription Factors
(徳島大学機関リポジトリ): ● Metadata: 117194
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.celrep.2022.110384
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35172142; ● Search Scopus @ Elsevier (PMID): 35172142; ● Search Scopus @ Elsevier (DOI): 10.1016/j.celrep.2022.110384

(徳島大学機関リポジトリ: 117194, DOI: 10.1016/j.celrep.2022.110384, PubMed: 35172142) Hitoshi Nishijima, Minoru Matsumoto, Junko Morimoto, Kazuyoshi Hosomichi, Nobuko Akiyama, Taishin Akiyama, Takeshi Oya, Koichi Tsuneyama, Hideyuki Yoshida and Mitsuru Matsumoto :
Aire Controls Heterogeneity of Medullary Thymic Epithelial Cells for the Expression of Self-Antigens.,
The Journal of Immunology, Vol.208, No.2, 303-320, 2022.

(要約): The deficiency of Aire, a transcriptional regulator whose defect results in the development of autoimmunity, is associated with reduced expression of tissue-restricted self-Ags (TRAs) in medullary thymic epithelial cells (mTECs). Although the mechanisms underlying Aire-dependent expression of TRAs need to be explored, the physical identification of the target(s) of Aire has been hampered by the low and promiscuous expression of TRAs. We have tackled this issue by engineering mice with augmented Aire expression. Integration of the transcriptomic data from Aire-augmented and Aire-deficient mTECs revealed that a large proportion of so-called Aire-dependent genes, including those of TRAs, may not be direct transcriptional targets downstream of Aire. Rather, Aire induces TRA expression indirectly through controlling the heterogeneity of mTECs, as revealed by single-cell analyses. In contrast, Ccl25 emerged as a canonical target of Aire, and we verified this both in vitro and in vivo. Our approach has illuminated the Aire's primary targets while distinguishing them from the secondary targets.
(キーワード): Animals / Autoantigens / Autoimmunity / Chemokines, CC / Epithelial Cells / Gene Expression Regulation / Gene Knock-In Techniques / Gene Knockout Techniques / Mice / Mice, Inbred C57BL / Mice, Inbred NOD / Mice, Transgenic / Thymus Gland / Transcription Factors / Transcription, Genetic
(徳島大学機関リポジトリ): ● Metadata: 117482
(出版サイトへのリンク): ● Publication site (DOI): 10.4049/jimmunol.2100692
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34930780; ● Search Scopus @ Elsevier (PMID): 34930780; ● Search Scopus @ Elsevier (DOI): 10.4049/jimmunol.2100692

(徳島大学機関リポジトリ: 117482, DOI: 10.4049/jimmunol.2100692, PubMed: 34930780) Mayuko Shimizu, Yosuke Tsuchiyama, Yuki Morimoto, Minoru Matsumoto, Tomoko Kobayashi, Satoshi Sumida, Takumi Kakimoto, Takeshi Oya, Hirohisa Ogawa, Michiko Yamashita, Satoru Matsuda, Katsuhisa Omagari, Shu Taira and Koichi Tsuneyama :
A novel mouse model of non-alcoholic steatohepatitis suggests that liver fibrosis initiates around lipid-laden macrophages,
The American Journal of Pathology, Vol.192, No.1, 31-42, 2022.

(要約): Various cells, such as macrophages and hepatic stellate cells, interact in the generation of fibrosis in nonalcoholic steatohepatitis (NASH), but the mechanism remains unclear. We employed a high-fat/cholesterol/cholate (HFCC) diet to generate a model of NASH-related fibrosis and investigate the pathogenesis of fibrosis. Two mouse strains differing in susceptibility to obesity, the susceptible strain C57BL/6J and the relatively resistant strain A/J, developed hepatic histologic features of NASH, including fat deposition, intralobular inflammation, hepatocyte ballooning, and fibrosis, after 9 weeks of HFCC diet feeding. The severity of hepatic inflammation and fibrosis was greater in A/J mice than in C57BL/6J mice. A/J mice fed the HFCC diet exhibited characteristic CD204-positive lipid-laden macrophage aggregation in hepatic parenchyma. Polarized light visualized the Maltese cross (namely, cholesterol crystals within the aggregated macrophages). Moreover, fibrosis developed in a ring shape from the periphery of the aggregated macrophages (ie, the starting point of fibrosis could be visualized histologically). Furthermore, matrix-assisted laser desorption/ionization mass spectrometry imaging analysis detected a molecule at m/z 772.462, which corresponds to the protonated ion of phosphatidylcholine [P-18:1 (11Z)/18:0] and phosphatidylethanolamine [18:0/20:2 (11Z, 14Z)], in aggregated macrophages adjacent to the fibrotic lesions. In conclusion, the present HFCC diet-fed A/J model provides an ideal tool to study fibrogenesis and enables novel insights into the pathophysiology of NASH-related fibrosis.
(キーワード): Liver fibrosis / マクロファージ (macrophage) / animal model / コレステロール (cholesterol) / cholate
(徳島大学機関リポジトリ): ● Metadata: 116411
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.ajpath.2021.10.002
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34710382; ● Search Scopus @ Elsevier (PMID): 34710382; ● Search Scopus @ Elsevier (DOI): 10.1016/j.ajpath.2021.10.002

(徳島大学機関リポジトリ: 116411, DOI: 10.1016/j.ajpath.2021.10.002, PubMed: 34710382) Mayuko Shimizu, Takeshi Kageyama, Takeshi Oya, Hirohisa Ogawa, Minoru Matsumoto, Satoshi Sumida, Takumi Kakimoto, Yuko Miyakami, Ryosuke Nagatomo, Koichi Inoue, Chunmei Cheng and Koichi Tsuneyama :
Verification of the Impact of Blood Glucose Level on Liver Carcinogenesis and the Efficacy of a Dietary Intervention in a Spontaneous Metabolic Syndrome Model,
International Journal of Molecular Sciences, Vol.22, No.23, 12844, 2021.

(要約): Metabolic syndrome (MS) is a risk factor for type 2 diabetes mellitus, vascular inflammation, atherosclerosis, and renal, liver, and heart diseases. Non-alcoholic steatohepatitis (NASH) is a progressive representative liver disease and may lead to the irreversible calamities of cirrhosis and hepatocellular carcinoma. Metabolic disorders such as hyperglycemia have been broadly reported to be related to hepatocarcinogenesis in NASH; however, direct evidence of a link between hyperglycemia and carcinogenesis is still lacking. Tsumura Suzuki Obese Diabetic (TSOD) mice spontaneously develop metabolic syndrome, including obesity, insulin resistance, and NASH-like liver phenotype, and eventually develop hepatocellular carcinomas. TSOD mice provide a spontaneous human MS-like model, even with significant individual variations. In this study, we monitored mice in terms of their changes in blood glucose levels, body weights, and pancreatic and liver lesions over time. As a result, liver carcinogenesis was delayed in non-hyperglycemic TSOD mice compared to hyperglycemic mice. Moreover, at the termination point of 40 weeks, liver tumors appeared in 18 of 24 (75%) hyperglycemic TSOD mice; in contrast, they only appeared in 5 of 24 (20.8%) non-hyperglycemic mice. Next, we investigated three kinds of oligosaccharide that could lower blood glucose levels in hyperglycemic TSOD mice. We monitored the levels of blood and urinary glucose and assessed pancreatic lesions among the experimental groups. As expected, significantly lower levels of blood and urinary glucose and smaller deletions of Langerhans cells were found in TSOD mice fed with milk-derived oligosaccharides (galactooligosaccharides and lactosucrose). At the age of 24 weeks, mild steatohepatitis was found in the liver but there was no evidence of liver carcinogenesis. Steatosis in the liver was alleviated in the milk-derived oligosaccharide-administered group. Taken together, suppressing the increase in blood glucose level from a young age prevented susceptible individuals from diabetes and the onset of NAFLD/NASH, as well as carcinogenesis. Milk-derived oligosaccharides showed a lowering effect on blood glucose levels, which may be expected to prevent liver carcinogenesis.
(徳島大学機関リポジトリ): ● Metadata: 116736
(出版サイトへのリンク): ● Publication site (DOI): 10.3390/ijms222312844
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34884650; ● Search Scopus @ Elsevier (PMID): 34884650; ● Search Scopus @ Elsevier (DOI): 10.3390/ijms222312844

(徳島大学機関リポジトリ: 116736, DOI: 10.3390/ijms222312844, PubMed: 34884650) Tomoko Kobayashi, Mayuko Shimizu, Takeshi Oya, Hirohisa Ogawa, Minoru Matsumoto, Yuki Morimoto, Satoshi Sumida, Takumi Kakimoto, Michiko Yamashita, Mitsuko Sutoh, Shunji Toyohara, Ryoji Hokao, Chunmei Cheng and Koichi Tsuneyama :
Neonatal streptozotocin treatment rapidly causes different subtype of hepatocellular carcinoma without persistent hyperglycemia in 4CS mice fed on a normal diet.,
Pathology, Research and Practice, Vol.225, No.153559, 2021.

(要約): Although diabetes mellitus (DM) is a well-known risk factor for hepatocellular carcinoma (HCC), the underlying mechanisms have not yet to be defined. We previously reported that DIAR mice fed with standard murine diet developed type 1 diabetes and HCC at age of 16 weeks old with a neonatal streptozotocin treatment (n-STZ). Because DIAR mice did not manifest obesity nor develop steatohepatitis, hyperglycemia with streptozotocin trigger or streptozotocin alone might turn on the hepato-carcinogenesis. An insulin-recruitment to DIAR-nSTZ mice showed an increased frequency of HCC during the first 12 weeks of age, although the diabetic indications notably improved. To elucidate the role of hyperglycemia in hepato-carcinogenesis, we performed a head-to-head comparative study by using 4CS mice and DIAR mice with n-STZ treatment. Newborn 4CS mice and DIAR mice were divided into STZ treated group and control group. The blood glucose levels of DIAR-nSTZ mice increased at age of eight weeks, while that of 4CS-nSTZ mice were maintained in the normal range. At eight weeks old, three out of five DIAR-nSTZ mice (60%) and one out of ten 4CS-nSTZ mice (10%) developed multiple liver tumors. At age of 12 weeks old, all eight of DIAR-nSTZ mice (100%) and two of 10 4CS-nSTZ mice (20%) developed multiple liver tumors. At 16 weeks old, all animals of DIAR-nSTZ and 4CS-nSTZ mice occurred liver tumors. DIAR-nSTZ showed hyperglycemia and HCC, and 4CS-nSTZ developed HCC without hyperglycemia. These results were interpreted that the onset of HCC maybe not related to the presence or absence of hyperglycemia but nSTZ treatment. On the other hand, since the carcinogenesis of 4CS-nSTZ is delayed compared to DIAR-nSTZ, hyperglycemia may play a role in the progression of carcinogenesis. Histologically, the liver tumor appeared irregularly trabecular arrangements of hepatocytes with various degrees of nuclear atypia. By immunohistochemical analyses, all liver tumors showed positive staining of glutamine synthetase (GS), an established human HCC marker. The expression pattern of GS was divided into a strong diffuse pattern and weak patchy pattern, respectively. The liver tumor showing the weak GS-patchy pattern expressed biliary/stem markers, EpCAM, and SALL4, partially. Because 4CS-nSTZ mice did not show any metabolic complications such as gaining body weight or high blood glucose level, it is a unique animal model with a simple condition to investigate hepatic carcinogenesis by excluding other factors.
(徳島大学機関リポジトリ): ● Metadata: 118286
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.prp.2021.153559
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34325313; ● Search Scopus @ Elsevier (PMID): 34325313; ● Search Scopus @ Elsevier (DOI): 10.1016/j.prp.2021.153559

(徳島大学機関リポジトリ: 118286, DOI: 10.1016/j.prp.2021.153559, PubMed: 34325313) Yuki Morimoto, Takeshi Oya, Mayuko Shimizu, Minoru Matsumoto, Hirohisa Ogawa, Tomoko Kobayashi, Satoshi Sumida, Takumi Kakimoto, Michiko Yamashita, Chunmei Cheng and Koichi Tsuneyama :
Applying Probe Electrospray Ionization Mass Spectrometry to Cytological Diagnosis: A Preliminary Study by Using Cultured Lung Cancer Cells.,
Acta Cytologica, Vol.65, No.5, 430-439, 2021.

(要約): PESI-MS presented a promising potential as a novel diagnostic modality for swiftly acquiring specific cytological information.
(徳島大学機関リポジトリ): ● Metadata: 116345
(出版サイトへのリンク): ● Publication site (DOI): 10.1159/000516639
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34098551; ● Search Scopus @ Elsevier (PMID): 34098551; ● Search Scopus @ Elsevier (DOI): 10.1159/000516639

(徳島大学機関リポジトリ: 116345, DOI: 10.1159/000516639, PubMed: 34098551) Ferreirinha Pedro, Ribeiro Camila, Junko Morimoto, Landry J M Jonathan, Minoru Matsumoto, Meireles Catarina, White J Andrea, Izumi Ohigashi, Araújo Leonor, Benes Vladimir, Yousuke Takahama, Anderson Graham, Mitsuru Matsumoto and Alves L Nuno :
A novel method to identify Post-Aire stages of medullary thymic epithelial cell differentiation,
European Journal of Immunology, Vol.51, No.2, 311-318, 2021.

(要約): Autoimmune regulator (Aire) medullary thymic epithelial cells (mTECs) play a critical role in tolerance induction. Several studies demonstrated that Aire mTECs differentiate further into Post-Aire cells. Yet, the identification of terminal stages of mTEC maturation depends on unique fate-mapping mouse models. Herein, we resolve this limitation by segmenting the mTEC (MHCII CD80 ) compartment into mTEC (CD24 Sca1 ), mTEC (CD24 Sca1 ), and mTEC (CD24 Sca1 ). While mTEC included mostly Aire-expressing cells, mTEC contained Aire and Aire cells and mTEC were mainly composed of cells lacking Aire. The differential expression pattern of Aire led us to investigate the precursor-product relationship between these subsets. Strikingly, transcriptomic analysis of mTEC , mTEC , and mTEC sequentially mirrored the specific genetic program of Early-, Late- and Post-Aire mTECs. Corroborating their Post-Aire nature, mTEC downregulated the expression of tissue-restricted antigens, acquired traits of differentiated keratinocytes, and were absent in Aire-deficient mice. Collectively, our findings reveal a new and simple blueprint to survey late stages of mTEC differentiation.
(キーワード): Animals / Cell Differentiation / Down-Regulation / Epithelial Cells / Gene Expression Profiling / Gene Expression Regulation / Keratinocytes / Mice / Mice, Inbred C57BL / Thymus Gland / Transcription Factors
(徳島大学機関リポジトリ): ● Metadata: 116300
(出版サイトへのリンク): ● Publication site (DOI): 10.1002/eji.202048764
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32845012; ● Summary page in Scopus @ Elsevier: 2-s2.0-85090990353

(徳島大学機関リポジトリ: 116300, DOI: 10.1002/eji.202048764, PubMed: 32845012, Elsevier: Scopus) Minoru Matsumoto, Koichi Tsuneyama, Junko Morimoto, Kazuyoshi Hosomichi, Mitsuru Matsumoto and Hitoshi Nishijima :
Tissue-specific autoimmunity controlled by Aire in thymic and peripheral tolerance mechanisms.,
International Immunology, Vol.32, No.2, 117-131, 2020.

(要約): Tissue-specific autoimmune diseases are assumed to arise through malfunction of two checkpoints for immune tolerance: defective elimination of autoreactive T cells in the thymus and activation of these T cells by corresponding autoantigens in the periphery. However, evidence for this model and the outcome of such alterations in each or both of the tolerance mechanisms have not been sufficiently investigated. We studied these issues by expressing human AIRE (huAIRE) as a modifier of tolerance function in NOD mice wherein the defects of thymic and peripheral tolerance together cause type I diabetes (T1D). Additive huAIRE expression in the thymic stroma had no major impact on the production of diabetogenic T cells in the thymus. In contrast, huAIRE expression in peripheral antigen-presenting cells (APCs) rendered the mice resistant to T1D, while maintaining other tissue-specific autoimmune responses and antibody production against an exogenous protein antigen, because of the loss of Xcr1+ dendritic cells, an essential component for activating diabetogenic T cells in the periphery. These results contrast with our recent demonstration that huAIRE expression in both the thymic stroma and peripheral APCs resulted in the paradoxical development of muscle-specific autoimmunity. Our results reveal that tissue-specific autoimmunity is differentially controlled by a combination of thymic function and peripheral tolerance, which can be manipulated by expression of huAIRE/Aire in each or both of the tolerance mechanisms.
(徳島大学機関リポジトリ): ● Metadata: 114944
(出版サイトへのリンク): ● Publication site (DOI): 10.1093/intimm/dxz066
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31586207; ● Search Scopus @ Elsevier (PMID): 31586207; ● Search Scopus @ Elsevier (DOI): 10.1093/intimm/dxz066

(徳島大学機関リポジトリ: 114944, DOI: 10.1093/intimm/dxz066, PubMed: 31586207) Junko Morimoto, Yumiko Nishikawa, Takumi Kakimoto, Kohei Furutani, Naoki Kihara, Minoru Matsumoto, Koichi Tsuneyama, Yuko Kozono, Haruo Kozono, Katsuto Hozumi, Kazuyoshi Hosomichi, Hitoshi Nishijima and Mitsuru Matsumoto :
Aire Controls in Trans the Production of Medullary Thymic Epithelial Cells Expressing Ly-6C/Ly-6G.,
The Journal of Immunology, Vol.201, No.11, 3244-3257, 2018.

(要約): Medullary thymic epithelial cells (mTECs), which express a wide range of tissue-restricted Ags (TRAs), contribute to the establishment of self-tolerance by eliminating autoreactive T cells and/or inducing regulatory T cells. Aire controls a diverse set of TRAs within Aire-expressing cells by employing various transcriptional pathways. As Aire has a profound effect on transcriptomes of mTECs, including TRAs not only at the single-cell but also the population level, we suspected that Aire (Aire+ mTECs) might control the cellular composition of the thymic microenvironment. In this study, we confirmed that this is indeed the case by identifying a novel mTEC subset expressing Ly-6 family protein whose production was defective in Aire-deficient thymi. Reaggregated thymic organ culture experiments demonstrated that Aire did not induce the expression of Ly-6C/Ly-6G molecules from mTECs as Aire-dependent TRAs in a cell-intrinsic manner. Instead, Aire+ mTECs functioned in trans to maintain Ly-6C/Ly-6G+ mTECs. Thus, Aire not only controls TRA expression transcriptionally within the cell but also controls the overall composition of mTECs in a cell-extrinsic manner, thereby regulating the transcriptome from mTECs on a global scale.
(出版サイトへのリンク): ● Publication site (DOI): 10.4049/jimmunol.1800950
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30389776; ● Search Scopus @ Elsevier (PMID): 30389776; ● Search Scopus @ Elsevier (DOI): 10.4049/jimmunol.1800950

(DOI: 10.4049/jimmunol.1800950, PubMed: 30389776)

MISC

Yosuke Iwakawa, Masaaki Nishi, Yuuma Wada, Kouzou Yoshikawa, Chie Takasu, Mitsuo Shimada, Yasuyo Saijo, Minoru Matsumoto, Takeshi Oya and Hisanori Uehara :
Pleomorphic type undifferentiated gastric sarcoma, report of a case.,
Clinical Journal of Gastroenterology, Vol.16, No.1, 20-25, 2022.

(要約): Reports on pleomorphic type of undifferentiated sarcoma (PUS) originating from the gastrointestinal tract, especially the stomach, are extremely rare. We herein report a case of pleomorphic type undifferentiated gastric sarcoma. The patient was a 67-year-old woman. The chief complaint was upper abdominal pain. Upper gastrointestinal endoscopy, ultrasonography, and contrast-enhanced computed tomography showed two submucosal tumors at the greater curvature of the fundus and the lesser curvature of the gastric angle. Endoscopic ultrasound-guided fine-needle aspiration revealed a c-kit-negative spindle cell tumor at the greater curvature of the fundus. Total gastrectomy, splenectomy, and partial resection of the diaphragm and liver were performed. One lesion had invaded the lateral segment of the liver, left diaphragm and spleen. The postoperative course was uneventful. Histopathological and immunohistochemical examinations of the resected specimen revealed PUS. Peritoneal dissemination was detected at 8 months after surgery. However, no effective therapeutic agents were adopted for chemotherapy. The patient had poor performance status due to disease progression and underwent best supportive care. The patient died 10 months after surgery. This case highlights the imaging, histological diagnosis, and treatment strategy for PUS originating from the stomach. Surgeons should be aware of PUS as a differential diagnosis in cases with submucosal tumor of the stomach.
(キーワード): Female / Humans / Aged / Stomach Neoplasms / Gastrectomy / Sarcoma / Endoscopy, Digestive System / Liver Neoplasms
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s12328-022-01729-y
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36289170; ● Search Scopus @ Elsevier (PMID): 36289170; ● Search Scopus @ Elsevier (DOI): 10.1007/s12328-022-01729-y

(DOI: 10.1007/s12328-022-01729-y, PubMed: 36289170)

総説・解説

常山幸一, 松本穣, 米田亜樹子, 尾矢剛志 :
【肝細胞性腫瘍の分類・亜分類の最前線】肝細胞腺腫肝細胞腺腫の分類と分子生物学的成り立ち(解説/特集),
肝·胆·膵, Vol.80, No.4, 691-699, 2020年4月. 常山幸一, 尾矢剛志, 小川博久, 松本穣, 佐竹宣法 :
【自己免疫性肝疾患-自己免疫性肝炎，原発性胆汁性胆管炎，原発性硬化性胆管炎-】発症機序，病理自己免疫性肝炎自己免疫性肝炎の病理(解説/特集),
日本臨牀, Vol.78, No.1, 65-70, 2020年1月. 常山幸一, 清水真祐子, 尾矢剛志, 松本穣, 小林智子, 小川博久, 西辻和親, 山下理子 :
肝臓病理所見のとり方とその解釈,
法医病理, Vol.25, No.1, 1-12, 2019年7月. 松本穣, 常山幸一, 松本満 :
AIRE遺伝子と多腺性自己免疫症候群,
最新医学, Vol.73, No.5, 688-692, 2018年5月.

講演・発表

Takumi Kakimoto, Mayuko Shimizu, Koichi Tsuneyama, Minoru Matsumoto, Takeshi Oya, Hosokawa Masato and Koichi Tsuneyama :
Accumulation of α-synuclein in hepatocytes in NASH liver and usefulness in pathological diagnosis,
Digestive Disease Week 2022, May 2022. Minoru Matsumoto, Mitsuru Matsumoto, Junko Morimoto and Hitoshi Nishijima :
Tissue-specific Autoimmunity Controlled by Aire, a Gene Responsible for APECED,
The 3rd International Congress on Rare Diseases, Berlin, Germany, Mar. 2020. Minoru Matsumoto, Hitoshi Nishijima, Ryuichiro Miyazawa, Junko Morimoto, Koichi Tsuneyama and Mitsuru Matsumoto :
Characterization of Aire-expressing DCs with high-sensitivity and high-fidelity Aire-reporter strain,
The 48th Annual Meeting of the Japanese Society for Immunology, Hamamatsu, Japan, Dec. 2019. Mayuko Shimizu, Hirohisa Ogawa, Minoru Matsumoto and Koichi Tsuneyama :
Establishment of a novel dietary-induced mouse model showing steatohepatitis with severe fibrosis,
UEG Week 2019, Barcelona, Oct. 2019. Mitsuru Matsumoto, Junko Morimoto, Minoru Matsumoto, Koichi Tsuneyama, Ryuichiro Miyazawa and Hitoshi Nishijima :
Aire-dependent establishment of self-tolerance,
The 17th International Congress of Immunology, Beijing, Oct. 2019. Minoru Matsumoto and Mitsuru Matsumoto :
Tissue-specific autoimmunity controlled by Aire in thymic and peripheral tolerance mechanisms,
The 18th Awaji International Forum on Infection and Immunity, Awaji, Japan, Sep. 2019. Mitsuru Matsumoto, Junko Morimoto, Minoru Matsumoto, Koichi Tsuneyama, Ryuichiro Miyazawa and Hitoshi Nishijima :
Aire-dependent establishment of self-tolerance studied by genetically modified mice,
EMBO Workshop ThymE, Israel, May 2019. Minoru Matsumoto, Junko Morimoto, Mitsuru Matsumoto and Hitoshi Nishijima :
Tissue-specific autoimmunity modified by Aire in thymic and peripheral tolerance,
5th International Congress on Controversies in Rheumatology and Autoimmunity (CORA), Italy, Mar. 2019. Mitsuru Matsumoto, Minoru Matsumoto, Junko Morimoto, Koichi Tsuneyama and Hitoshi Nishijima :
Tissue-specific autoimmunity manipulated by Aire in thymic and peripheral tolerance,
Immunology of Diabetes Society Congress 2018, London, Oct. 2018. Mitsuru Matsumoto, Junko Morimoto, Minoru Matsumoto and Hitoshi Nishijima :
Aire controls in trans the production of medullary thymic epithelial cells expressing Ly6C/Ly6G,
5th European Congress of Immunology 2018, Amsterdam, Sep. 2018. 西條康代, 常山幸一, 松本穣, 尾矢剛志 :
悪性転化を来した biliary adenofibroma の1例,
第113回日本病理学会総会, 2024年3月. 松本穣 :
シングルセル解析を用いた胸腺上皮細胞ならびに胸腺癌へのアプローチ,
第113回日本病理学会総会先端的分子病理学講習会, 2024年3月. 松本穣, 西條康代, 尾矢剛志 :
S2900,
日本病理学会中国四国支部学術集会(Web開催)第142回スライドカンファレンス, 2023年11月. 西條康代, 尾矢剛志, 松本穣 :
S2883 下垂体腫瘍,
日本病理学会中国四国支部学術集会(Web開催)第141回スライドカンファレンス, 2023年6月. 厚美憲吾, 松本穣, 山下理子, 西村碧フィリーズ, 佐藤康晴, 坂東良美, 上原久典 :
リンパ節病変,
第141回日本病理学会中国四国支部学術集会スライドカンファレンス, 2023年6月.

(キーワード): 成人T細胞白血病

松本穣, 西條康代, 清水真祐子, 小川博久, 常山幸一, 松本満, 尾矢剛志 :
胸腺癌におけるAIRE発現と胸腺髄質上皮細胞との類似性,
日本病理学会会誌, Vol.111, No.1, 243, 2022年4月. 松本穣, 松本満, 尾矢剛志 :
胸腺癌におけるAIRE発現と胸腺髄質上皮細胞との類似性,
第41回日本胸腺研究会, 2022年2月. Minoru Matsumoto, Hitoshi Nishijima, Junko Morimoto, Koichi Tsuneyama and Mitsuru Matsumoto :
Aire controls heterogeneity of medullary thymic epithelial cells for the expression of self-antigens,
第50回日本免疫学会学術集会, Dec. 2021. Junko Morimoto, Minoru Matsumoto, Ryuichiro Miyazawa and Mitsuru Matsumoto :
Aire suppresses CTLA-4 expression from medullary thymic epithelial cells to avoid autoimmunity.,
第50回日本免疫学会学術集会, Dec. 2021. 柿本拓海, 清水真祐子, 小川博久, 松本穣, 尾矢剛志, 常山幸一 :
⾮アルコール性脂肪性肝炎の診断におけるα -synuclein 免疫組織化学染⾊の有⽤性,
The 67th Autumn Annual Meeting of Japanese Society of Pathology, 2021年11月. 宮上侑子, 松本穣, 工藤英治, 佐竹宣法, 常山幸一, 尾矢剛志 :
膵神経内分泌腫瘍の一剖検例,
第67回日本病理学会秋期特別総会, 2021年11月. 西條康代, 坂東良美, 尾矢剛志, 松本穣, 上原久典 :
S2838 頭蓋内腫瘍,
日本病理学会中国四国支部学術集会第136回スライドカンファレンス, 2021年10月. 廣兼百合, 松本穣, 常山幸一, 尾矢剛志 :
von Hippel-Lindau病に関連したendolymphatic sac tumorの一例,
第110回日本病理学会総会, 2021年4月. 檜本朱成, 松本穣, 工藤英治, 常山幸一, 尾矢剛志 :
NF1患者に発症した多発性消化管間質腫瘍の1例,
第110回日本病理学会総会, 2021年4月. 住田智志, 清水真祐子, 西條康代, 松本穣, 小川博久, 尾矢剛志, 坂東良美, 上原久典, 常山幸一 :
膵内副脾発生類表皮嚢胞の発生機序・組織学的特徴に関する検討,
第110回日本病理学会総会, 2021年4月. 松本穣, 尾矢剛志, 松本満 :
Aireレポーターマウスを用いた胸腺内Aire発現樹状細胞の解析,
第40回日本胸腺研究会, 2021年2月. 木内華由, 松本穣, 常山幸一, 尾矢剛志 :
胃腫瘍,
日本病理学会中国四国支部学術集会第133回スライドカンファレンス(Web開催), 2020年11月. 吉田光輝, 近藤和也, 北市隆, 尾矢剛志, 松本穣, 宮本直輝, 南城和正, 庄野隆志, 牧秀則, 山本清成, 坂本晋一, 髙嶋美佳, 松本大資, 河北直也, 鳥羽博明, 川上行奎, 滝沢宏光, 丹黒章 :
分類不能型縦隔高悪性度腫瘍の手術例の経験,
第73回日本胸部外科学会定期学術集会(Web開催), 2020年10月. 溝渕海, 吉田光輝, 近藤和也, 北市隆, 尾矢剛志, 松本穣, 竹原恵美, 宮本直輝, 髙嶋美佳, 松本大資, 河北直也, 坪井光弘, 鳥羽博明, 川上行奎, 滝沢宏光, 丹黒章 :
前縦隔に発生した分類不能型高悪性度腫瘍の一切除例,
第37回日本呼吸器外科学会学術集会(Web開催), 2020年9月. 宮田晃志, 宮澤龍一郎, 松本穣, 松本満 :
AIRE発現樹状細胞の機能解析,
第109回日本病理学会総会, 2020年7月. 松本穣, 西嶋仁, 松本満, 常山幸一 :
ヒトAIREトランスジェニックマウスに認めた糖尿病抵抗性獲得機構の解析,
第109回日本病理学会総会, 2020年7月. 清水真祐子, 平修, 松本穣, 尾矢剛志, 小川博久, 常山幸一 :
イメージング質量分析によるNASH線維化肝で増加する脂質の同定,
第109回日本病理学会総会, 2020年7月. 廣兼百合, 尾矢剛志, 松本穣, 常山幸一 :
側頭骨腫瘍,
日本病理学会中国四国支部学術集会第132回スライドカンファレンス, 2020年6月. 吉田光輝, 近藤和也, 北市隆, 尾矢剛志, 松本穣, 宮本直輝, 鈴木恵美, 高嶋美佳, 松本大資, 河北直也, 坪井光弘, 鳥羽博明, 川上行奎, 滝沢宏光, 丹黒章 :
前縦隔に発生した分類不能型高悪性度腫瘍の一切除例,
第39回日本胸腺研究会, 2020年2月. 清水真祐子, 平修, 松本穣, 尾矢剛志, 小川博久, 常山幸一 :
NASH線維化肝におけるpathogen lipidsの同定,
第260回徳島医学会学術集会, 2020年2月. 西嶋仁, 杉田瑞季, 森本純子, 松本穣, 松本満 :
Aireを高発現する胸腺髄質上皮細胞の免疫学的機能とトランスクリプトーム解析,
第42回日本分子生物学会年会, 2019年12月. 常山幸一, 清水真祐子, 尾矢剛志, 松本穣, 小川博久 :
自然発症メタボリックシンドローム-NASH-HCCモデルマウスにおけるプレバイオティクスによる腸内細菌叢への介入効果の検討,
第30回日本消化器癌発生学会総会, 2019年11月. 尾矢剛志, 松本穣, 香川典子, 山下理子, 小川博久, 常山幸一 :
小腸腫瘍の1例,
日本病理学会中国四国支部学術集会第130回スライドカンファレンス, 2019年10月. 小林智子, 上原久典, 松本穣, 坂東良美 :
急速に進行する呼吸不全を呈し，acute fibrinous and organizing pneumonia が示唆された一剖検例,
第108回日本病理学会総会, 2019年5月. 松本穣, 小林智子, 坂東良美, 上原久典 :
膀胱癌の進展における脂肪由来因子の関与,
第108回日本病理学会総会, 2019年5月. 尾矢剛志, 松本穣, 小川博久, 常山幸一 :
胃病変,
日本病理学会中国四国支部学術集会第128回スライドカンファレンス, 2019年2月. Hitoshi Nishijima, Junko Morimoto, Minoru Matsumoto and Mitsuru Matsumoto :
Transcriptomic analysis of medullary thymic epithelial cells with augmented Aire expression,
第47回日本免疫学会学術集会, Dec. 2018. Junko Morimoto, Hitoshi Nishijima, Minoru Matsumoto and Mitsuru Matsumoto :
Analysis of the role of thymic APCs and Aire in the production of thymic Tregs,
第47回日本免疫学会学術集会, Dec. 2018. 常山幸一, 清水真祐子, 尾矢剛志, 松本穣, 小川博久 :
異なる系統で作成したストレプトゾトシン誘導肝細胞癌モデルマウスの病態比較,
第29回日本消化器癌発生学会総会, 2018年11月. 西嶋仁, 森本純子, 松本穣, 松本満 :
胸腺髄質上皮細胞における Aire 発現レベルと組織特異的自己抗原遺伝子発現との関連性に関する検討,
28 Kyoto T cell Conference (KTCC), 2018年6月.

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補助金・競争的資金: 空間的シングルセル解析による胸腺癌の病態解明 (研究課題/領域番号: 23K14478 )
胸腺トレランスをめぐる２課題の解決 (研究課題/領域番号: 22K19437 )
AIREによる糖尿病抵抗性獲得機構の実験病理学的解析 (研究課題/領域番号: 19K16613 )
AIREを基軸とする自己免疫疾患の病態解明、ならびに新規治療法の開発 (研究課題/領域番号: 19H03699 )
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受賞: 2020年8月, 日本病理学会100周年記念病理学研究新人賞 (社団法人日本病理学会)
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Jグローバル最終確認日: 2024/4/27 01:28
氏名（漢字）: 松本穣
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氏名（英字）: Matsumoto Minoru
所属機関: 徳島大学大学院医歯薬学研究部講師

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researchmap最終確認日: 2024/4/28 02:01
氏名（漢字）: 松本穣
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所属: 徳島大学大学院医歯薬学研究部
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研究者番号: 30836250

所属（現在）: 2024/4/1 : 徳島大学, 大学院医歯薬学研究部(医学域), 講師

所属（過去の研究課題 情報に基づく）*注記: 2021/4/1 – 2023/4/1 : 徳島大学, 大学院医歯薬学研究部(医学域), 講師
2019/4/1 – 2020/4/1 : 徳島大学, 大学院医歯薬学研究部(医学域), 助教

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小区分49030:実験病理学関連
小区分49020:人体病理学関連

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小区分54020:膠原病およびアレルギー内科学関連
中区分49:病理病態学、感染・免疫学およびその関連分野
小区分49070:免疫学関連

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AIRE / I型糖尿病 / Xcr1陽性樹状細胞 / NOD / Ⅰ型糖尿病 / 糖尿病 / 胸腺癌 / 胸腺上皮性腫瘍 / 空間的シングルセル解析

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自己免疫疾患 / AIRE / 遺伝子改変マウス / 胸腺 / I型糖尿病 / 自己寛容 / Aire / 自己抗原 / 転写因子

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