Tokushima University / Educator and Researcher Directory --- Sato-Fukuba, Mami

Personal Web Page

https://orcid.org/0000-0002-5606-1684 (ORCID)

Field of Study

○	Pathology and Immunology

Subject of Study

○

Book / Paper

Book:

1.	Kunihiro Otsuka, Takaaki Tsunematsu, Aya Ushio, Mami Sato and Naozumi Ishimaru : シェーグレン症候群の病理, Oct. 2022.

Academic Paper (Judged Full Paper):

1.	富田満, Hirohisa Ogawa, Takaaki Tsunematsu, Mami Sato, 山下貴央, Yoshiaki Kitamura, Naozumi Ishimaru, Koichi Tsuneyama, Hisanori Uehara and Yoshimi Bando : 線維化と腫瘍随伴リンパ組織増生を伴う粘表皮癌の1例, 診断病理, Vol.40, No.4, 336-341, 2023.
2.	Mami Sato-Fukuba, Rieko Arakaki, Aya Ushio, Kunihiro Otsuka, Ruka Nagao, Shigefumi Matsuzawa, Hiroaki Tawara, Takaaki Tsunematsu and Naozumi Ishimaru : CD4 T-cell-dependent differentiation of CD23 follicular B cells contributes to the pulmonary pathology in a primary Sjögren's syndrome mouse model., Frontiers in Immunology, Vol.14, 1217492, 2023. (Summary) Primary Sjögren's syndrome (pSS) is a systemic autoimmune disease that affects the function of exocrine glands, such as the lacrimal and the salivary glands. Extraglandular lesions and malignant lymphoma also occur during the progressive stage of pSS. We have, herein, focused on the pulmonary lesions of pSS and have aimed clarifying their pathophysiological mechanism by comparing the glandular with the extraglandular lesions observed in a mouse model of pSS. The histopathological analysis of lung tissues obtained from NFS/ mice that have undergone neonatal thymectomy was performed. Moreover, and experiments were conducted along with immunological analyses in order to characterize the unique phenotypes of the pulmonary lesions identified in these pSS model mice. Inflammatory lesions with a bronchus-associated lymphoid tissue-like structure were identified in the lungs of pSS model mice. In addition, relative to salivary gland lesions, pulmonary lesions showed increased CD23 follicular B (FB) cells. and pulmonary B cells were more readily driven to CD23 FB cell phenotype than salivary gland B cells in pSS model mice. Furthermore, the CD23 FB cell differentiation was found to be enhanced in a CD4 T-cell-dependent manner under a Th2-type condition in the lungs of herein examined pSS model mice. A Th2-type response in the pSS lung may promote the progression of autoimmune lesions through an enhanced abnormal differentiation of B cells. (Keyword) Mice / Animals / Sjögren's syndrome / salivary glands / B-Lymphocytes / cell differentiation / CD4-Positive T-Lymphocytes (Tokushima University Institutional Repository) ● Metadata: 118467 (Link to Publication Site) ● Publication site (DOI): 10.3389/fimmu.2023.1217492 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37475871 ● Summary page in Scopus @ Elsevier: 2-s2.0-85165185874 (Tokushima University Institutional Repository: 118467, DOI: 10.3389/fimmu.2023.1217492, PubMed: 37475871, Elsevier: Scopus)
3.	Mami Sato, Rieko Arakaki, Hiroaki Tawara, Ruka Nagao, Hidetaka Tanaka, Kai Tamura, Yuki Kawahito, Aya Ushio, Takaaki Tsunematsu and Naozumi Ishimaru : Disturbed natural killer cell homeostasis in the salivary gland enhances autoimmune pathology via IFN-γ in a mouse model of primary Sjogren's syndrome., Frontiers in Medicine, Vol.9, 1036787, 2022. (Summary) Innate lymphoid cells (ILCs), including natural killer (NK) cells, ILC1, ILC2, lymphoid tissue-inducer (LTi) cells, and ILC3 cell, play a key role in various immune responses. Primary Sjögren's syndrome (pSS) is an autoimmune disease characterized by chronic inflammation of exocrine glands, such as the lacrimal and salivary glands (SGs). The role of NK cells among ILCs in the pathogenesis of pSS is still unclear. In this study, the characteristics and subsets of NK cells in the salivary gland (SG) tissue were analyzed using a murine model of pSS. Multiple phenotypes and cytotoxic signature of the SG NK cells in control and pSS model mice were evaluated by flow cytometric analysis. Intracellular expression of interferon-γ (IFN-γ) among T cells and NK cells from the SG tissues was compared by experiments. In addition, pathological analysis was performed using anti-asialo-GM1 (ASGM1) antibody (Ab)-injected pSS model mice. The number of conventional NK (cNK) cells in the SG of pSS model mice significantly increased compared with that in control mice at 6 weeks of age. The production level of IFN-γ was significantly higher in SG NK cells than in SG T cells. The depletion of NK cells by ASGM1 Ab altered the ratio of tissue resident NK (rNK) cells to cNK cells, which inhibited the injury to SG cells with the recovery of saliva secretion in pSS model mice. The results indicate that SG cNK cells may enhance the autoreactive response in the target organ by upregulating of IFN-γ, whereas SG rNK cells protect target cells against T cell cytotoxicity. Therefore, the activation process and multiple functions of NK cells in the target organ could be helpful to develop potential markers for determining autoimmune disease activity and target molecules for incurable immune disorders. (Tokushima University Institutional Repository) ● Metadata: 118305 (Link to Publication Site) ● Publication site (DOI): 10.3389/fmed.2022.1036787 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36388880 ● Search Scopus @ Elsevier (PMID): 36388880 ● Search Scopus @ Elsevier (DOI): 10.3389/fmed.2022.1036787 (Tokushima University Institutional Repository: 118305, DOI: 10.3389/fmed.2022.1036787, PubMed: 36388880)
4.	Takaaki Tsunematsu, Rieko Arakaki, Mami Sato, Masako Saito, Kunihiro Otsuka, Furukawa Yusuke, Taquahashi Yuhji, Kanno Jun and Naozumi Ishimaru : Exposure to Multiwall Carbon Nanotubes Promotes Fibrous Proliferation by Production of Matrix Metalloproteinase-12 via NF-κB Activation in Chronic Peritonitis., The American Journal of Pathology, Vol.S0002-9440, No.22, 00240, 2022. (Summary) The toxicologic effects of nanomaterials, such as carbon nanotubes (CNTs), on the immune system are considerably understood. However, the precise relationship between long-term exposure to CNTs and chronic inflammation remains unclear. In this study, a mouse model of chronic peritonitis was established using i.p. injection of multiwalled CNTs treated by the Taquann method with high dispersion efficiency. Chronic peritonitis with fibrosis was observed in Taquann-treated multiwalled CNT (T-CNT)-injected mice, but not in Taquann-treated titanium dioxide-injected mice. In vivo and in vitro experiments showed that matrix metalloproteinase-12 (MMP-12) of macrophages was up-regulated by T-CNT to enhance fibroblast activation and profibrotic molecule expression in fibroblasts. In addition, T-CNT-induced peritonitis reduced MMP-12 expression in Nfκb1 mice, suggesting that MMP-12-producing macrophages play a key role in chronic inflammation due to T-CNT exposure through NF-κB activation. The results of this study could be helpful in understanding the molecular toxicity of nanomaterial and chronic inflammation. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ajpath.2022.07.009 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35963465 ● Search Scopus @ Elsevier (PMID): 35963465 ● Search Scopus @ Elsevier (DOI): 10.1016/j.ajpath.2022.07.009 (DOI: 10.1016/j.ajpath.2022.07.009, PubMed: 35963465)
5.	Kunihiro Otsuka, Mami Sato, Takaaki Tsunematsu and Naozumi Ishimaru : Virus Infections Play Crucial Roles in the Pathogenesis of Sjögren's Syndrome., Viruses, Vol.14, No.7, 1474, 2022. (Summary) Sjögren's syndrome (SS) is an autoimmune disease especially targeting exocrine glands, such as the salivary and lacrimal glands. A radical therapy for SS based on its etiology has not been established because of the complex pathogenesis of the disease. Several studies have demonstrated a relationship between virus infection and SS pathogenesis. In particular, infection with the Epstein-Barr (EB) virus among others is a potent factor associated with the onset or development of SS. Specifically, virus infection in the target organs of SS triggers or promotes autoreactive responses involving the process of autoantigen formation, antigen-presenting function, or T-cell response. Our review of recent research highlights the crucial roles of virus infection in the pathogenesis of SS and discusses the critical association between virus infection and the etiology of autoimmunity in SS. (Keyword) Autoantigens / autoimmunity / Herpesvirus 4, Human / Humans / Sjögren's syndrome / Virus Diseases (Tokushima University Institutional Repository) ● Metadata: 117727 (Link to Publication Site) ● Publication site (DOI): 10.3390/v14071474 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35891453 ● Summary page in Scopus @ Elsevier: 2-s2.0-85133687255 (Tokushima University Institutional Repository: 117727, DOI: 10.3390/v14071474, PubMed: 35891453, Elsevier: Scopus)
6.	Mami Sato, Rieko Arakaki, Hiroaki Tawara, Takaaki Tsunematsu and Naozumi Ishimaru : Formation of Autoimmune Lesions Is Independent of Antibiotic Treatment in NOD Mice., International Journal of Molecular Sciences, Vol.22, No.6, 3239, 2021. (Summary) The relationship between autoimmunity and changes in intestinal microbiota is not yet fully understood. In this study, the role of intestinal microbiota in the onset and progression of autoimmune lesions in non-obese diabetic (NOD) mice was evaluated by administering antibiotics to alter their intestinal microenvironment. Flow cytometric analysis of spleen cells showed that antibiotic administration did not change the proportion or number of T and B cells in NOD mice, and pathological analysis demonstrated that autoimmune lesions in the salivary glands and in the pancreas were also not affected by antibiotic administration. These results suggest that the onset and progression of autoimmunity may be independent of enteral microbiota changes. Our findings may be useful for determining the appropriate use of antibiotics in patients with autoimmune diseases who are prescribed drugs to maintain systemic immune function. (Keyword) Animals / Anti-Bacterial Agents / Autoimmune Diseases / autoimmunity / cytokinesis / Disease Models, Animal / Disease Susceptibility / Immune System / Mice / Mice, Inbred NOD / Sialadenitis (Tokushima University Institutional Repository) ● Metadata: 117463 (Link to Publication Site) ● Publication site (DOI): 10.3390/ijms22063239 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33810172 ● Search Scopus @ Elsevier (PMID): 33810172 ● Search Scopus @ Elsevier (DOI): 10.3390/ijms22063239 (Tokushima University Institutional Repository: 117463, DOI: 10.3390/ijms22063239, PubMed: 33810172)
7.	Kunihiro Otsuka, Akiko Yamada, Masako Saito, Aya Ushio, Mami Sato, Satoru Kisoda, Wenhua Shao, Takaaki Tsunematsu, Yasusei Kudo, Rieko Arakaki and Naozumi Ishimaru : Ascl2-Regulated Follicular Helper T Cells Promote Autoimmunity in a Murine Model for Sjögren's Syndrome., The American Journal of Pathology, Vol.189, No.12, 2414-2427, 2019. (Summary) mice that received neonatal thymectomy treatment demonstrated that Ascl2 contributes to the Tfh cell differentiation associated with autoimmunity during the early stages independent of Bcl6. In conclusion, our results indicate that abnormal Tfh cell differentiation via Ascl2 regulation might contribute to the pathogenesis of autoimmunity. (Keyword) Animals / Autoantibodies / autoimmunity / B-Lymphocytes / Basic Helix-Loop-Helix Transcription Factors / cell differentiation / Cytokines / Disease Models, Animal / female / Germinal Center / Mice / Mice, Inbred C57BL / Proto-Oncogene Proteins c-bcl-6 / Sjögren's syndrome / T-Lymphocytes, Helper-Inducer (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ajpath.2019.08.008 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31539517 ● Summary page in Scopus @ Elsevier: 2-s2.0-85075213858 (DOI: 10.1016/j.ajpath.2019.08.008, PubMed: 31539517, Elsevier: Scopus)
8.	Rieko Arakaki, Aya Ushio, Satoru Kisoda, Mami Sato, Yoshitaka Nakamura, Kanako Yuyama, Riho Tateyama, Satoru Morishita, Noriyuki Monoi, Yasusei Kudo and Naozumi Ishimaru : Novel effects of rooibos extract on tear and saliva secretion mediated by the muscarinic acetylcholine receptor 3 in mice, Journal of Oral Biosciences, Vol.61, No.3, 179-182, 2019. (Summary) Sicca syndrome is characterized by dry mouth and eyes and results in a reduction of the patient's quality of life. Various natural plants, including certain herbs, have long been employed to alleviate such symptoms. Rooibos grown in South Africa is one of the potent herbal plants used for the treating dry mouth. However, the precise mechanism of action by which rooibos alleviates symptoms of dryness remains unclear. The in vivo effects of rooibos extract (RE), which comprises eriodictyol-6-C-glucoside, on the secretory function of saliva and tears were analyzed after intraoral RE administration using wild-type C57BL/6 (B6) mice. In addition, the mechanisms of RE were investigated after administration of a muscarinic acetylcholine receptor 3 (M3R) antagonist. Tear and saliva volumes in mice increased significantly and in a dose-dependent manner following intraoral RE administration compared to those in mice in the control group administered HO. An experiment performed using darifenacin administration revealed that the effects of RE on secretory function were exerted via M3R. These results suggest that RE administration is an effective treatment for symptoms of dryness and may be used in clinical settings against sicca syndrome. (Keyword) Animals / Aspalathus / Humans / Mice / Mice, Inbred C57BL / Plant Extracts / Quality of Life / Receptors, Muscarinic / Saliva / South Africa (Link to Publication Site) ● Publication site (DOI): 10.1016/j.job.2019.06.001 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31400544 ● Summary page in Scopus @ Elsevier: 2-s2.0-85070548928 (DOI: 10.1016/j.job.2019.06.001, PubMed: 31400544, Elsevier: Scopus)

Proceeding of Domestic Conference:

1.	Mami Sato-Fukuba, NISHIDA Mari, Masahiko Watanabe, Kohei Naniwa, Kohichi Kani, Yukihiro Momota and Keiko Aota : 1型糖尿病モデルマウス唾液腺における発現遺伝子の網羅的解析, 第21回日本口腔ケア学会総会・学術大会第4回国際口腔ケア学会総会・学術大会, Apr. 2024.
2.	富田満, Hidehisa Horiguchi, Hirohisa Ogawa, Hisanori Uehara, Yoshimi Bando, Takaaki Tsunematsu, Mami Sato, Naozumi Ishimaru and Koichi Tsuneyama : CRTC1::MAML2融合遺伝子の検出で確定診断に至った粘表皮癌の2例, 第113回日本病理学会総会, Mar. 2024.
3.	Kai Tamura, KAWAHITO Yuki, Mami Sato, Kunihiro Otsuka, Aya Ushio, Takaaki Tsunematsu and Naozumi Ishimaru : Pathological analysis of nasal lesions with aging in murine models of Sjögrens syndrome, 第52回日本免疫学会総会・学術集会, Jan. 2024.
4.	KAWAHITO Yuki, Tamura Kai, Mami Sato, Kunihiro Otsuka, Aya Ushio, Takaaki Tsunematsu and Naozumi Ishimaru : The Relation between the Reduction of Mucin 19 and the Onset of Sjögrens syndrome in a Mouse Model, 第52回日本免疫学会総会・学術集会, Jan. 2024.
5.	Keiko Aota, Kohichi Kani, 西田真理, Mami Sato-Fukuba, Kohei Naniwa and Yukihiro Momota : JAK阻害薬バリシチニブは唾液腺導管細胞のIFN-γ誘導性CXCL10発現を抑制する, 第59回日本口腔組織培養学会総会・学術大会, Nov. 2023.
6.	Kohei Naniwa, Mami Sato-Fukuba, 西田真理 (名), 大山博行 (名), Kohichi Kani, Yukihiro Momota and Keiko Aota : 当科における自己免疫性水疱症の臨床的検討, 第68回日本口腔外科学会総会・学術大会, Nov. 2023.
7.	Kohichi Kani, 西田真理, 大山博行, Mami Sato-Fukuba, Kohei Naniwa, Hideyuki Takano, Yukihiro Momota and Keiko Aota : 上唇に発生した嚢胞腺腫の1例, 第68回口腔外科学会総会・学術大会, Nov. 2023.
8.	Mami Sato-Fukuba, Kohei Naniwa, Kohichi Kani, Yukihiro Momota and Keiko Aota : 不明熱を契機にシェーグレン症候群の診断に至った7歳女児例, 第70回 NPO法人日本口腔科学会中国・四国地方部会, Oct. 2023.
9.	Kohichi Kani, 西田真理, Masahiko Watanabe, 大山博行, Mami Sato-Fukuba, Kohei Naniwa, Yukihiro Momota and Keiko Aota : 急激な増大を呈した頬粘膜形質芽細胞性リンパ腫の1例, 第33回日本口腔内科学会・4学会合同学術大会, Sep. 2023.
10.	Kohei Naniwa, 大山博行, 西田真理, Mami Sato-Fukuba, Kohichi Kani, Yukihiro Momota and Keiko Aota : 多形滲出性紅斑の1例, 第52回口腔外科学会中四国支部学術大会, Jul. 2023.
11.	Kai Tamura, Yuki KAWAHITO, Mami Sato, Kunihiro Otsuka, Takaaki Tsunematsu and Naozumi Ishimaru : シェーグレン症候群モデルマウスにおける加齢に伴う鼻腔病変の病態解析, 第112回日本病理学会総会, Apr. 2023.
12.	Yuki KAWAHITO, Kai Tamura, Mami Sato, Kunihiro Otsuka, Takaaki Tsunematsu and Naozumi Ishimaru : シェーグレン症候群疾患モデルマウスにおけるMucin19の異常と病態との関連性の解析, 第112回日本病理学会総会, Apr. 2023.
13.	Takaaki Tsunematsu, Hiroaki TAWARA, Mami Sato, Kazuki FUKUTA, Kunihiro Otsuka, Aya Ushio and Naozumi Ishimaru : DNA損傷シグナルによって誘導されるがん細胞の新たな機能とその分子機構, 第112回日本病理学会総会, Apr. 2023.
14.	Hiroaki TAWARA, Takaaki Tsunematsu, Kazuki FUKUTA, RUKA Nagao, Mami Sato, Kunihiro Otsuka, Aya Ushio and Naozumi Ishimaru : 染色体パッセンジャー複合体構成因子Borealin-Survivin相互作用は頭頸部扁平上皮癌の代謝を制御する, 第112回日本病理学会総会, Apr. 2023.
15.	Kunihiro Otsuka, Hiroyuki Kondo, Shin-ichi Tsukumo, Rieko Arakaki, Ruka Nagao, Mami Sato, Aya Ushio, Naozumi Ishimaru and Koji Yasutomo : CD153-CD30相互反応を介したシェーグレン症候群の病態形成機構の解明, 第112回日本病理学会総会, Apr. 2023.
16.	Hiroaki TAWARA, Takaaki Tsunematsu, Nagao RUKA, Kazuki FUKUTA, Mami Sato, Kunihiro Otsuka, Aya Ushio and Naozumi Ishimaru : 頭頸部扁平上皮癌における染色体パッセンジャー複合体構成因子Borealinの高発現がもたらす新たな役割, 第58回日本口腔組織培養学会学術大会・総会, Dec. 2022.
17.	Mami Sato, Aya Ushio, Kunihiro Otsuka, Takaaki Tsunematsu and Naozumi Ishimaru : Th2 response enhances the differentiation into follicular B cells to progress the pulmonary autoimmune lesions in a mouse model of Sjögrens syndrome, 第51回日本免疫学会学術集会, Dec. 2022.
18.	Kunihiro Otsuka, Shin-ichi Tsukumo, Rieko Arakaki, Mami Sato, 八木田秀雄, Naozumi Ishimaru and Koji Yasutomo : CD153+ CD4+ T cells exacerbate the autoimmune pathology via the interaction with CD30+ cells in salivary glands in Sjögren's syndrome., 第51回日本免疫学会学術集会, Dec. 2022.
19.	Kai Tamura, Yuki KAWAHITO, Mami Sato, Kunihiro Otsuka, Takaaki Tsunematsu and Naozumi Ishimaru : Pathological analysis of nasal tissue in a murine model of Sjögrens syndrome, 第51回日本免疫学会学術集会, Dec. 2022.
20.	Yuki KAWAHITO, Kai Tamura, Mami Sato, Kunihiro Otsuka, Takaaki Tsunematsu and Naozumi Ishimaru : Role of Mucin 19 in Pathogenesis of a Mouse Model for Sjögren's Syndrome, 第51回日本免疫学会学術集会, Dec. 2022.
21.	Takaaki Tsunematsu, Rieko Arakaki, Mami Sato, Kunihiro Otsuka and Naozumi Ishimaru : Exposure to Multi-Wall Carbon Nanotubes Promotes Fibrous Proliferation by Production of Matrix Metalloproteinase-12 via NF-κB Activation in Chronic Peritonitis, 第51回日本免疫学会学術集会, Dec. 2022.
22.	Hiroaki TAWARA, Takaaki Tsunematsu, RUKA Nagao, Mami Sato, Kunihiro Otsuka and Naozumi Ishimaru : がんにおける染色体パッセンジャー複合体構成因子Borealinの高発現がもたらす新たな機能, 第45回日本分子生物学学会年会, Dec. 2022.
23.	Kunihiro Otsuka, Hiroyuki Kondo, Shin-ichi Tsukumo, Rieko Arakaki, Mami Sato, Takaaki Tsunematsu, Naozumi Ishimaru and Koji Yasutomo : シングルセルRNA-seqとマルチプレックスSpatial解析を基盤としたシェーグレン症候群の標的臓器微小環境変化の解明, 第33回日本臨床口腔病理学会, Sep. 2022.
24.	Takaaki Tsunematsu, Hiroaki TAWARA, Mami Sato, Rieko Arakaki, Kunihiro Otsuka, Aya Ushio and Naozumi Ishimaru : 頭頸部扁平上皮癌における染色体パッセンジャー複合体構成因子Borealinの新たな機能, 第64回歯科基礎医学会学術大会, Sep. 2022.
25.	Yuki KAWAHITO, Kai Tamura, Mami Sato, Kunihiro Otsuka, Takaaki Tsunematsu and Naozumi Ishimaru : シェーグレン症候群モデルマウスであるNFS/sldマウスの変異遺伝子Mucin19の発現解析と病態との関連性, 第64回歯科基礎医学会学術大会, Sep. 2022.
26.	Kunihiro Otsuka, Shin-ichi Tsukumo, Hiroyuki Kondo, Mami Sato, Hiroaki TAWARA, Takaaki Tsunematsu, Naozumi Ishimaru and Koji Yasutomo : シングルセルRNA-seqで紐解くシェーグレン症候群モデルに特徴的に出現するT細胞集団の解析, 第64回歯科基礎医学会学術大会, Sep. 2022.
27.	Kai Tamura, Yuki KAWAHITO, Mami Sato, Kunihiro Otsuka, Takaaki Tsunematsu and Naozumi Ishimaru : シェーグレン症候群モデルマウスにおける鼻腔組織の病態解析, 第64回歯科基礎医学会学術大会, Sep. 2022.
28.	Mami Sato, Aya Ushio, Kunihiro Otsuka, Takaaki Tsunematsu and Naozumi Ishimaru : シェーグレン症候群モデルマウス肺病変におけるケモカインの機能分析, 第64回歯科基礎医学会学術大会, Sep. 2022.
29.	Mami Sato, Aya Ushio, Kunihiro Otsuka, Takaaki Tsunematsu and Naozumi Ishimaru : シェーグレン症候群疾患モデルマウスの肺病変における濾胞B細胞の自己反応性獲得機構の解明, 先端歯学国際教育研究ネットワーク先端歯学スクール, Aug. 2022.
30.	Mami Sato, Aya Ushio, Kazuki FUKUTA, Hiroaki TAWARA, Kunihiro Otsuka, Takaaki Tsunematsu, Rieko Arakaki and Naozumi Ishimaru : Extraglandular lesions in Sjogren's syndorome model mice., 第20回四国免疫フォーラム, Jun. 2022.
31.	Mami Sato, Aya Ushio, Kunihiro Otsuka, Takaaki Tsunematsu, Rieko Arakaki and Naozumi Ishimaru : シェーグレン症候群モデルマウス肺病変に対するケモカイン群の機能的解析, 第20回四国免疫フォーラム, Jun. 2022.
32.	Takaaki Tsunematsu, Hiroaki TAWARA, Hidetaka TANAKA, Kazuki FUKUTA, Mami Sato, Kunihiro Otsuka, Rieko Arakaki and Naozumi Ishimaru : 口腔扁平上皮癌におけるBorealinの高発現がもたらすSurvivin安定化機構の解明, 第111回日本病理学会総会, Apr. 2022.
33.	Mami Sato, Rieko Arakaki, Takaaki Tsunematsu, Yasusei Kudo and Naozumi Ishimaru : シェーグレン症候群疾患モデルにおける肺病変発症へのCCL6の役割, 第111回日本病理学会総会, Apr. 2022.
34.	Mami Sato, Takaaki Tsunematsu, Kunihiro Otsuka and Naozumi Ishimaru : 下顎骨病変, 日本病理学会中国四国支部学術集会 (第 137 回スライドカンファレンス), Feb. 2022.
35.	Kunihiro Otsuka, Shin-ichi Tsukumo, Rieko Arakaki, Mami Sato, Hideo Yagita, Naozumi Ishimaru and Koji Yasutomo : Single-cell RNA sequencing reveals accumulation of CD4 and CD8 T cells with unique phenotypes in salivary glands of Sjögren's syndrome model mice, 第50回日本免疫学会学術集会, Dec. 2021.
36.	Mami Sato, 牛尾綾, 福田一稀, 俵宏彰, Kunihiro Otsuka, Takaaki Tsunematsu, Rieko Arakaki and Naozumi Ishimaru : シェーグレン症候群モデルマウスにおける肺病変の病態探索, 第29回日本シェーグレン症候群学会学術集会, Sep. 2021.
37.	Kunihiro Otsuka, Akiko Yamada, Masako Saito, Aya Ushio, Mami Sato, Satoru Kisoda, Wenhua Shao, Takaaki Tsunematsu, Yasusei Kudo, Rieko Arakaki and Naozumi Ishimaru : Achaete-Scute Homologue 2-Regulated Follicular Helper T Cells Promote Autoimmunity in a Murine Model for Sjögren Syndrome., 第32回日本臨床口腔病理学会奨励賞(実験病理分野), Aug. 2021.
38.	Mami Sato, Aya Ushio, Kazuki FUKUTA, Hiroaki TAWARA, Kunihiro Otsuka, Takaaki Tsunematsu, Rieko Arakaki and Naozumi Ishimaru : シェーグレン症候群モデルマウスにおける腺外病変, 第19回四国免疫フォーラム, Jun. 2021.
39.	Mami Sato, 牛尾綾, Takaaki Tsunematsu, Rieko Arakaki and Naozumi Ishimaru : シェーグレン症候群モデルマウスにおける肺病変の解析, 第110回日本病理学会学術集会, Apr. 2021.
40.	Rieko Arakaki, 清水朱里, Mami Sato, 俵宏彰, Takaaki Tsunematsu and Naozumi Ishimaru : 唾液腺における常在型自然リンパ球の同定とシェーグレン症候群病態への関与, 第110回日本病理学会学術集会, Apr. 2021.
41.	Takaaki Tsunematsu, Takumi KITAGAWA, Mami Sato, Rieko Arakaki and Naozumi Ishimaru : HPV陽性扁平上皮癌細胞の生存に必須な脱ユビキチン化酵素の同定とその役割の解明, 第110回日本病理学会総会, Apr. 2021.
42.	Mami Sato, Aya Ushio, Rieko Arakaki, 俵宏彰, Takaaki Tsunematsu and Naozumi Ishimaru : シェーグレン症候群モデルマウスにおける腺外病変の発症機序, 四国歯学会第57回例会, Mar. 2021.
43.	Mami Sato, Takaaki Tsunematsu, Kunihiro Otsuka and Naozumi Ishimaru : 下顎骨病変, 日本病理学会中国四国支部学術集会第 137 回スライドカンファレンス, Feb. 2021.
44.	Mami Sato, Rieko Arakaki, Aya Ushio, Yasusei Kudo and Naozumi Ishimaru : Effect of mulyi-wall carbon nanotube exposure on pulmonary immune cells at the early stage., Proceedings of the Japanese Society for Immunology, Dec. 2019.
45.	Satoru Kisoda, Wenhua Shao, Aya Ushio, Mami Sato, Rieko Arakaki, Naozumi Ishimaru and Yasusei Kudo : 口腔癌におけるpartial-EMTに関する遺伝子の悪性度への関与, 第38回分子病理研究会, Jul. 2019.

Et cetera, Workshop:

1.	林亜門, 清水朱里, 中西美緒, 山内加奈, Mami Sato, 邵文華, 木曽田暁, Hitomi Fukui, 木野倫子, Aya Ushio, Akiko Yamada, Takaaki Tsunematsu, Rieko Arakaki, Yasusei Kudo and Naozumi Ishimaru : 口腔分子病態学分野における免疫・癌研究, 徳島県歯科医学大会(四国歯学会第56回例会), Feb. 2020.
2.	Satoru Kisoda, Bunka Sho, Aya Ushio, Mami Sato, Rieko Arakaki, Naozumi Ishimaru and Yasusei Kudo : 口腔癌におけるpartial-EMTに関連する遺伝子の悪性度への関与, 第38回分子病理学研究会, Jul. 2019.

Assistant Professor : Sato-Fukuba, Mami

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