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• Analysis of Development and Function of T Cell Receptor Gamma Delta T Cells

• Analysis of Host Defense Mechanism against Infections and Vaccine Development

• Immunoregulation in mycobacterial infection

Published Papers 【 display / non-display 】

Published Papers 【 display / non-display 】

• GRIM-19 is a target of mycobacterial Zn2+ metalloprotease 1 and indispensable for NLRP3 inflammasome activation.

  Kurane T, Matsunaga T, Ida T, Sawada K, Nishimura A, , Fukui M, Umemura1 M, Nakayama M, Ohara N, Matsumoto S, Akaike T, Matsuzaki G, Takaesu G

  FASEB Journal ( Wiley )  36 ( 1 ) e22096   2022.10 [ Peer Review Accepted ]

  Type of publication: Research paper (scientific journal)

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• Heat-killed Lactobacillus plantarum L-137 attenuates obesity and associated metabolic abnormalities in C57BL/6 J mice on a high-fat diet.

  Yoshitake R, Hirose Y, Murosaki S, Matsuzaki G.

  Bioscience of Microbiota, Food and Health   40 ( 2 ) 84 - 91   2021.04 [ Peer Review Accepted ]

  Type of publication: Research paper (scientific journal)

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• TREM2 is a receptor for non-glycosylated mycolic acids of mycobacteria that limits anti-mycobacterial macrophage activation.

  Iizasa E, Chuma Y, Uematsu T, Kubota M, Kawaguchi H, Umemura M, Toyonaga K, Kiyohara H, Yano I, Colonna M, Sugita M, Matsuzaki G, Yamasaki S, Yoshida H, Hara H.

  Nature Communications ( Nature Communications )  12 ( 1 ) 2299 - 2299   2021.04 [ Peer Review Accepted ]

  Type of publication: Research paper (scientific journal)

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  Mycobacterial cell-wall glycolipids elicit an anti-mycobacterial immune response via FcRγ-associated C-type lectin receptors, including Mincle, and caspase-recruitment domain family member 9 (CARD9). Additionally, mycobacteria harbor immuno-evasive cell-wall lipids associated with virulence and latency; however, a mechanism of action is unclear. Here, we show that the DAP12-associated triggering receptor expressed on myeloid cells 2 (TREM2) recognizes mycobacterial cell-wall mycolic acid (MA)-containing lipids and suggest a mechanism by which mycobacteria control host immunity via TREM2. Macrophages respond to glycosylated MA-containing lipids in a Mincle/FcRγ/CARD9-dependent manner to produce inflammatory cytokines and recruit inducible nitric oxide synthase (iNOS)-positive mycobactericidal macrophages. Conversely, macrophages respond to non-glycosylated MAs in a TREM2/DAP12-dependent but CARD9-independent manner to recruit iNOS-negative mycobacterium-permissive macrophages. Furthermore, TREM2 deletion enhances Mincle-induced macrophage activation in vitro and inflammation in vivo and accelerates the elimination of mycobacterial infection, suggesting that TREM2-DAP12 signaling counteracts Mincle-FcRγ-CARD9-mediated anti-mycobacterial immunity. Mycobacteria, therefore, harness TREM2 for immune evasion.

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• Mycobacterium bovis BCG-mediated suppression of Th17 response in mouse experimental autoimmune encephalomyelitis.

  Matsuzaki G, Teruya N, Kiyohara Kohama H, Arai K, Shibuya Y, Chuma Y, Matsuo K.

  Immunopharmacology and Immunotoxicology ( Informa UK Limited )  42 ( 2 ) 203 - 211   2021 [ Peer Review Accepted ]

  Type of publication: Research paper (scientific journal)

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  INTRODUCTION: Multiple sclerosis (MS) is an autoimmune disease mediated by a pro-inflammatory immune response. Experimental autoimmune encephalomyelitis (EAE) induced by immunization of mice with a myelin oligodendrocyte glycoprotein (MOG) peptide emulsified in killed Mycobacterium tuberculosis-containing complete Freund's adjuvant (CFA-EAE) is used as a model of MS. Mycobacterium bovis BCG has been reported to ameliorate clinical symptoms of CFA-EAE, although the precise mechanism has not yet been documented. Since CFA-EAE uses adjuvant with mycobacterial antigens, mycobacterial antigen-specific T cells induced by CFA may cross-react with BCG and modulate EAE. METHODS: To exclude the influence of cross-reactivity, a modified murine EAE model (cell wall skeleton (CWS)-EAE) that does not induce mycobacterial antigen-specific T cells was established and used to reevaluate the therapeutic effects of BCG on EAE. RESULTS: Inoculation with BCG 6 d after CWS-EAE induction successfully ameliorated EAE symptoms, suggesting that the therapeutic effects of BCG are independent of the mycobacterial antigen-specific T cells induced by the CFA-EAE protocol. BCG inoculation into the CWS-EAE mice resulted in reduced levels of MOG-specific Th17 in the central nervous system (CNS) with reduced demyelinated lesions of the spinal cord. In the draining lymph nodes of the MOG-immunized sites, BCG inoculation resulted in an increase in MOG-specific Th17 and Th1 cells at an early stage of immune response. CONCLUSION: The results suggest that BCG inoculation suppresses the Th17 response in the CNS of EAE mice via a mechanism that may involve the suppression of egress of encephalitogenic T cells from lymphoid organs.

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• Heat-killed Lactobacillus plantarum L-137 attenuates obesity and associated metabolic abnormalities in C57BL/6 J mice on a high-fat diet.

  Yoshitake R, Hirose Y, Murosaki S, Matsuzaki G

  Bioscience of microbiota, food and health ( BMFH出版会 )  40 ( 2 ) 84 - 91   2021 [ Peer Review Accepted ]

  Type of publication: Research paper (scientific journal)

  　View Summary

  <p>Heat-killed <i>Lactobacillus plantarum</i> L-137 (HK L-137) has anti-allergic, antitumor, and antiviral effects in mice, as well as an anti-inflammatory effect in rats with metabolic syndrome through regulation of immunity. To evaluate the influence of HK L-137 on chronic inflammation in mice with diet-induced obesity, C57BL/6 J mice were fed a normal diet (16% of energy as fat) or a high-fat diet (62% of energy as fat) with or without 0.002% HK L-137 for 4 to 20 weeks. It was found that HK L-137 supplementation alleviated weight gain and elevation of plasma glucose, cholesterol, alanine aminotransferase, and aspartate transaminase levels in mice with diet-induced obesity. Expression of several inflammation-related genes, including F4/80, CD11c, and IL-1β, in the epididymal adipose tissue of these mice was significantly downregulated by HK L-137. In addition, plasma levels of lipopolysaccharide-binding protein, a marker of endotoxemia, tended to be decreased by administration of HK L-137. These findings suggest that HK L-137 supplementation ameliorates obesity-induced metabolic abnormalities and adipose tissue inflammation, possibly through improvement of intestinal permeability.</p>

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Other Papers 【 display / non-display 】

Other Papers 【 display / non-display 】

• Dispensable role of chemokine receptors in migration of mycobacterial antigen specific CD4+T cells into mycobacteria-infected lung

  Umemura, M; Yamasaki, M; Tamura, T; Matsuzaki, G

  JOURNAL OF IMMUNOLOGY   204 ( 1 )   2020.05  [Refereed]

   

• マイコバクテリア感染肺に誘導されるIL‐17A産生細胞の多様性

  梅村正幸, 儀間香南子, 高江洲義一, 中江進, 岩倉洋一郎, 松崎吾朗

  日本インターフェロン・サイトカイン学会学術集会抄録集   83   96   2018.07

   

• アルツハイマー病脳内炎症の中核機構に迫る ITAM共役型受容体による抗酸菌脂質の認識と自然免疫応答の制御

  原 博満, 飯笹 英一, 清原 秀泰, 中馬 康志, 梅村 正幸, 山崎 晶, 松崎 吾朗, 吉田 裕樹

  Dementia Japan ( (一社)日本認知症学会 )  31 ( 4 ) 505 - 505   2017.10

   

• [ORIGINAL CONTRIBUTIONS]Impaired Th2 differentiation of CD4+ T cells from Rap2b knockout mice

  Uechi Yukiko, Matsuzaki Goro, Suzuki Masako, Asato Tsuyoshi, Takei Kimiko, Umikawa Masato, Oshiro Minoru, Maruyama Ichiro N, Endo Shogo, Kariya Ken-ichi, Department of Medical Biochemistry Graduate School of Medicine, Department of Infectious Diseases Tropical Biosphere Research Center, Neuroscience Research Team Tokyo Metropolitan Institute of Gerontology, Department of Medical Biochemistry Graduate School of Medicine, Department of Medical Biochemistry Graduate School of Medicine, Department of Medical Biochemistry Graduate School of Medicine, Department of Medical Biochemistry Graduate School of Medicine, Information Processing Biology Unit Okinawa Institute of Science and Technology Graduate University, Aging Neuroscience Research Team Tokyo Metropolitan Institute of Gerontology, Department of Medical Biochemistry Graduate School of Medicine

  琉球医学会誌 = Ryukyu Medical Journal ( 琉球医学会 )  34 ( 1 ) 45 - 52   2015.12  [Refereed]

   

• PAMPs受容体研究の最前線 自然免疫による結核菌ミコール酸脂質の認識

  原 博満, 飯笹 英一, 久保田 未央, 植松 崇之, 清原 秀泰, 山崎 晶, 松崎 吾朗, 吉田 裕樹

  日本細菌学雑誌 ( 日本細菌学会 )  70 ( 1 ) 128 - 128   2015.02

   

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Presentations 【 display / non-display 】

Presentations 【 display / non-display 】

• A novel role of GRIM-19 in cytokine production in macrophages upon mycobacterial infection

  Giichi Takaesu, Tomomi Kurane, Masayuki Umemura, Goro Matsuzaki

  2022.12  -  2022.12 

• Effect of Zmp1-deficient BCG vaccination in protective immunity to pulmonary tuberculosis

  Masayuki Umemura, Masayori Yoshisato, Ryusei Shimotada, Julia Toguchi, Giichi Takaesu, Goro Matsuzaki

  2022.12  -  2022.12 

• Analysis of Card9 function in pulmonary mycobacterial infection

  Kenji Toyonaga, Masayuki Umemura, Goro Matsuzaki, Hiromitsu Hara, Yoshihiko Tanaka, Sho Yamasaki

  2022.03  -  2022.03 

• GRIM-19 is a target of mycobacterial Zn2+ metalloprotease 1 and indispensable for NLRP3 inflammasome activation

  Tomomi Kurane, Masayuki Umemura, Masaaki Nakayama, Naoya Ohara, Goro Matsuzaki, Giichi Takaesu

  2021.12  -  2021.12 

• The effect of the deletion of the mycobacterial virulence factor Zmp1 on protective immunity

  Masayuki Umemura, Sohkichi Matsumoto, Tomomi Kurane, Giichi Takaesu, Goro Matsuzaki

  2021.12  -  2021.12 

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Grant-in-Aid for Scientific Research 【 display / non-display 】

Grant-in-Aid for Scientific Research 【 display / non-display 】

• Analysis of type 3 immune responses against M. tuberculosis infection and application to boost vaccine

  Grant-in-Aid for Scientific Research(C)

  Project Year: 2021.04  -  2024.03 

  Direct: 3,200,000 (YEN)  Overheads: 4,160,000 (YEN)  Total: 960,000 (YEN)

• Analysis of type 3 immune responses against M. tuberculosis infection and application to boost vaccine

  Grant-in-Aid for Scientific Research(C)

  Project Year: 2021.04  -  2024.03 

  Direct: 3,200,000 (YEN)  Overheads: 4,160,000 (YEN)  Total: 960,000 (YEN)

• Analysis of molecular mechanism of mitochondrial damage and immune suppression induced by Mycobacterium tuberculosis

  Grant-in-Aid for Scientific Research(B)

  Project Year: 2020.04  -  2023.03 

  Direct: 13,500,000 (YEN)  Overheads: 17,550,000 (YEN)  Total: 4,050,000 (YEN)

• Analysis of molecular mechanism of mitochondrial damage and immune suppression induced by Mycobacterium tuberculosis

  Grant-in-Aid for Scientific Research(B)

  Project Year: 2020.04  -  2023.03 

  Direct: 13,500,000 (YEN)  Overheads: 17,550,000 (YEN)  Total: 4,050,000 (YEN)

• Grant-in-Aid for Scientific Research(C)

  Project Year: 2018.04  -  2022.03 

  Direct: 3,300,000 (YEN)  Overheads: 4,290,000 (YEN)  Total: 990,000 (YEN)

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SDGs 【 display / non-display 】