徳島大学 / 教育研究者総覧 --- 牛尾綾

専門分野

○	口腔病理学 (Oral Pathology)

研究テーマ

○	シェーグレン症候群の病態解明 (シェーグレン症候群 (Sjögren's syndrome), 自己免疫疾患, 疾患モデルマウス)

著書・論文

著書:

1.	常松貴明, 俵宏彰, 大塚邦紘, 牛尾綾, 石丸直澄 : ヒトパピローマウイルス陽性がんにおける脱ユビキチン化酵素の役割, 日本口腔組織培養学会, 2022年11月.
2.	大塚邦紘, 常松貴明, 牛尾綾, 佐藤真美, 石丸直澄 : シェーグレン症候群の病理, 2022年10月.

学術論文(審査論文):

1.	Hiroaki Tawara, Takaaki Tsunematsu, Ruka Nagao, Shigefumi Matsuzawa, Kunihiro Otsuka, Aya Ushio and Naozumi Ishimaru : The noncanonical function of borealin, a component of chromosome passenger complex, promotes glycolysis via stabilization of survivin in squamous cell carcinoma cells., Biochemical and Biophysical Research Communications, Vol.706, 149741, 2024. (要約) The chromosome passenger complex (CPC) is a kinase complex formed by Aurora B, borealin, survivin and inner centromere protein (INCENP). The CPC is active during mitosis and contributes to proper chromosome segregation via the phosphorylation of various substrates. Overexpression of each CPC component has been reported in most cancers. However, its significance remains unclear, as only survivin is known to confer chemoresistance. This study showed that the overexpression of borealin, a CPC component, stabilized survivin protein depending on its interaction with survivin. Unexpectedly, the accumulation of survivin by borealin overexpression did not affect the well-characterized functions of survivin, such as chemoresistance and cell proliferation. Interestingly, the overexpression of borealin promoted lactate production but not the overexpression of the deletion mutant that lacks the ability to bind to survivin. Consistent with these findings, the expression levels of glycolysis-related genes were enhanced in borealin-overexpressing cancer cells. Meanwhile, the overexpression of survivin alone did not promote lactate production. Overall, the accumulation of the borealin-survivin complex promoted glycolysis in squamous cell carcinoma cells. This mechanism may contribute to cancer progression via excessive lactate production. (キーワード) Humans / Survivin / Centromere / Chromosomal Proteins, Non-Histone / Cell Cycle Proteins / Mitosis / Phosphorylation / Aurora Kinase B / Carcinoma, Squamous Cell / Lactates (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.bbrc.2024.149741 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38471204 ● Search Scopus @ Elsevier (PMID): 38471204 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2024.149741 (DOI: 10.1016/j.bbrc.2024.149741, PubMed: 38471204)
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. (要約) 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. (キーワード) Mice / Animals / シェーグレン症候群 (Sjögren's syndrome) / 唾液腺 (salivary glands) / B-Lymphocytes / 細胞分化 (cell differentiation) / CD4-Positive T-Lymphocytes (徳島大学機関リポジトリ) ● Metadata: 118467 (出版サイトへのリンク) ● Publication site (DOI): 10.3389/fimmu.2023.1217492 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37475871 ● Summary page in Scopus @ Elsevier: 2-s2.0-85165185874 (徳島大学機関リポジトリ: 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. (要約) 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. (徳島大学機関リポジトリ) ● Metadata: 118305 (出版サイトへのリンク) ● Publication site (DOI): 10.3389/fmed.2022.1036787 (文献検索サイトへのリンク) ● 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 (徳島大学機関リポジトリ: 118305, DOI: 10.3389/fmed.2022.1036787, PubMed: 36388880)
4.	Izumi Ohigashi, Melina Frantzeskakis, Alison Jacques, Sayumi Fujimori, Aya Ushio, Fusano Yamashita, Naozumi Ishimaru, Da Yin, Margaret Cam, C Michael Kelly, Parirokh Awasthi, Kensuke Takada and Yousuke Takahama : The thymoproteasome hardwires the TCR repertoire of CD8+ T cells in the cortex independent of negative selection., The Journal of Experimental Medicine, Vol.218, No.4, 2021. (要約) The thymoproteasome expressed specifically in thymic cortical epithelium optimizes the generation of CD8+ T cells; however, how the thymoproteasome contributes to CD8+ T cell development is unclear. Here, we show that the thymoproteasome shapes the TCR repertoire directly in cortical thymocytes before migration to the thymic medulla. We further show that the thymoproteasome optimizes CD8+ T cell production independent of the thymic medulla; independent of additional antigen-presenting cells, including medullary thymic epithelial cells and dendritic cells; and independent of apoptosis-mediated negative selection. These results indicate that the thymoproteasome hardwires the TCR repertoire of CD8+ T cells with cortical positive selection independent of negative selection in the thymus. (徳島大学機関リポジトリ) ● Metadata: 116455 (出版サイトへのリンク) ● Publication site (DOI): 10.1084/jem.20201904 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33555295 ● Search Scopus @ Elsevier (PMID): 33555295 ● Search Scopus @ Elsevier (DOI): 10.1084/jem.20201904 (徳島大学機関リポジトリ: 116455, DOI: 10.1084/jem.20201904, PubMed: 33555295)
5.	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. (要約) 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. (キーワード) Animals / Autoantibodies / 自己免疫 (autoimmunity) / B-Lymphocytes / Basic Helix-Loop-Helix Transcription Factors / 細胞分化 (cell differentiation) / Cytokines / Disease Models, Animal / 女性 (female) / Germinal Center / Mice / Mice, Inbred C57BL / Proto-Oncogene Proteins c-bcl-6 / シェーグレン症候群 (Sjögren's syndrome) / T-Lymphocytes, Helper-Inducer (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.ajpath.2019.08.008 (文献検索サイトへのリンク) ● 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)
6.	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. (要約) 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. (キーワード) Animals / Aspalathus / Humans / Mice / Mice, Inbred C57BL / Plant Extracts / Quality of Life / Receptors, Muscarinic / Saliva / South Africa (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.job.2019.06.001 (文献検索サイトへのリンク) ● 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)
7.	Aya Ushio, Rieko Arakaki, Kunihiro Ohtsuka, Akiko Yamada, Takaaki Tsunematsu, Yasusei Kudo, Keiko Aota, Masayuki Azuma and Naozumi Ishimaru : CCL22-Producing Resident Macrophages Enhance T Cell Response in Sjögren's Syndrome., Frontiers in Immunology, Vol.9, 2594, 2018. (要約) Macrophages (MΦs) are critical regulators of immune response and serve as a link between innate and acquired immunity. The precise mechanism of involvement of tissue-resident MΦs in the pathogenesis of autoimmune diseases is not clear. Here, using a murine model for Sjögren's syndrome (SS), we investigated the role of tissue-resident MΦs in the onset and development of autoimmunity. Two unique populations of CD11b and CD11b resident MΦs were observed in the target tissue of the SS model. Comprehensive gene expression analysis of chemokines revealed effective production of CCL22 by the CD11b MΦs. CCL22 upregulated the migratory activity of CD4 T cells by increasing CCR4, a receptor of CCL22, on T cells in the SS model. In addition, CCL22 enhanced IFN-γ production of T cells of the SS model, thereby suggesting that CCL22 may impair the local immune tolerance in the target organ of the SS model. Moreover, administration of anti-CCL22 antibody suppressed autoimmune lesions in the SS model. Finally, histopathological analysis revealed numerous CCL22-producing MΦs in the minor salivary gland tissue specimens of the SS patients. CCL22-producing tissue-resident MΦs may control autoimmune lesions by enhancing T cell response in the SS model. These results suggest that specific chemokines and their receptors may serve as novel therapeutic or diagnostic targets for SS. (徳島大学機関リポジトリ) ● Metadata: 113526 (出版サイトへのリンク) ● Publication site (DOI): 10.3389/fimmu.2018.02594 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30467506 ● Summary page in Scopus @ Elsevier: 2-s2.0-85056303968 (徳島大学機関リポジトリ: 113526, DOI: 10.3389/fimmu.2018.02594, PubMed: 30467506, Elsevier: Scopus)
8.	Kunihiro Ohtsuka, Kohichi Yamada, Yuhji Taquahashi, Rieko Arakaki, Aya Ushio, Masako Saito, Akiko Yamada, Takaaki Tsunematsu, Yasusei Kudo, Jun Kanno and Naozumi Ishimaru : Long-term polarization of alveolar macrophages to a profibrotic phenotype after inhalation exposure to multi-wall carbon nanotubes., PLoS ONE, Vol.13, No.10, e0205702., 2018. (要約) Nanomaterials are widely used in various fields. Although the toxicity of carbon nanotubes (CNTs) in pulmonary tissues has been demonstrated, the toxicological effect of CNTs on the immune system in the lung remains unclear. In this study, exposure to Taquann-treated multi-walled CNTs (T-CNTs) was performed using aerosols generated in an inhalation chamber. At 12 months after T-CNT exposure, alveolar inflammation with macrophage accumulation and hypertrophy of the alveolar walls were observed. In addition, fibrotic lesions were enhanced by T-CNT exposure. The macrophages in the bronchoalveolar lavage fluid of T-CNT-exposed mice were not largely shifted to any particular population, and were a mixed phenotype with M1 and M2 polarization. Moreover, the alveolar macrophages of T-CNT-exposed mice produced matrix metalloprotinase-12. These results suggest that T-CNT exposure promoted chronic inflammation and fibrotic lesion formation in profibrotic macrophages for prolonged periods. (徳島大学機関リポジトリ) ● Metadata: 113371 (出版サイトへのリンク) ● Publication site (DOI): 10.1371/journal.pone.0205702 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30372450 ● Summary page in Scopus @ Elsevier: 2-s2.0-85055616395 (徳島大学機関リポジトリ: 113371, DOI: 10.1371/journal.pone.0205702, PubMed: 30372450, Elsevier: Scopus)
9.	Aya Ushio, Rieko Arakaki, Hiroshi Eguchi, Fumika Hotta, Akiko Yamada, Yasusei Kudo and Naozumi Ishimaru : Pathological Analysis of Ocular Lesions in a Murine Model of Sjögren's Syndrome., International Journal of Molecular Sciences, Vol.18, No.6, 2017. (要約) Sjögren's syndrome (SS) is a systemic autoimmune disease characterized by severe inflammation of exocrine glands such as the salivary and lacrimal glands. When it affects the lacrimal glands, many patients experience keratoconjunctivitis due to severely dry eyes. This study investigated the pathological and immunological characteristics of ocular lesions in a mouse model of SS. Corneal epithelial injury and hyperplasia were confirmed pathologically. The number of conjunctival mucin-producing goblet cells was significantly decreased in the SS model mice compared with control mice. Expression levels of transforming growth factor (TGF)-, interleukin (IL)-6, tumor necrosis factor (TNF)-, and C-X-C motif chemokine (CXCL) 12 were significantly higher in the corneal epithelium of the SS model mice than in control mice. Inflammatory lesions were observed in the Harderian, intraorbital, and extraorbital lacrimal glands in the SS model mice, suggesting that the ocular glands were targeted by an autoimmune response. The lacrimal glands of the SS model mice were infiltrated by cluster of differentiation (CD)4+ T cells. Real-time reverse transcription-polymerase chain reaction (RT-PCR) revealed significantly increased mRNA expression of TNF-, TGF-, CXCL9, and lysozyme in the extraorbital lacrimal glands of the SS model mice compared with control mice. These results add to the understanding of the complex pathogenesis of SS and may facilitate development of new therapeutic strategies. (徳島大学機関リポジトリ) ● Metadata: 111713 (出版サイトへのリンク) ● Publication site (DOI): 10.3390/ijms18061209 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28587293 ● Search Scopus @ Elsevier (PMID): 28587293 ● Search Scopus @ Elsevier (DOI): 10.3390/ijms18061209 (徳島大学機関リポジトリ: 111713, DOI: 10.3390/ijms18061209, PubMed: 28587293)
10.	Satoko Kujiraoka, Takaaki Tsunematsu, Yukiko Sato, Maki Yoshida, Ayataka Ishikawa, Rei Tohyama, Michio Tanaka, Yutaka Kobayashi, Tomoyuki Kondo, Aya Ushio, Kunihiro Otsuka, Mie Kurosawa, Masako Saito, Akiko Yamada, Rieko Arakaki, Hirokazu Nagai, Hiromasa Nikai, Kengo Takeuchi, Toshitaka Nagao, Youji Miyamoto, Naozumi Ishimaru and Yasusei Kudo : Establishment and characterization of a clear cell odontogenic carcinoma cell line with EWSR1-ATF1 fusion gene., Oral Oncology, Vol.69, 46-55, 2017. (要約) To the best of our knowledge, this is the first report on the establishment of a CCOC cell line. CCOC-T cells serve as a useful in vitro model for understanding the pathogenesis and nature of MOT. (徳島大学機関リポジトリ) ● Metadata: 111726 (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.oraloncology.2017.04.003 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28559020 ● Search Scopus @ Elsevier (PMID): 28559020 ● Search Scopus @ Elsevier (DOI): 10.1016/j.oraloncology.2017.04.003 (徳島大学機関リポジトリ: 111726, DOI: 10.1016/j.oraloncology.2017.04.003, PubMed: 28559020)

国際会議:

1.	Kunihiro Ohtsuka, Akiko Yamada, Masako Saito, Aya Ushio, Takaaki Tsunematsu, Rieko Arakaki, Yasusei Kudo, Hidehiro Kishimmoto and Naozumi Ishimaru : Analysis of follicular helper T cells in a mouse model for Sjogren's Syndorome., 11th International Congress of Autoimmunity, Lisbon, May 2018.
2.	Aya Ushio, Rieko Arakaki, Kunihiro Ohtsuka, Yasusei Kudo and Naozumi Ishimaru : CCL22Producing Resident Macrophages Enhances InflaMMation in Salivary Glands of Sjogren's Syndorome., 11th International Congress of Autoimmunity, Lisbon, May 2018.
3.	Rieko Arakaki, Aya Ushio, Kunihiro Ohtsuka, Yasusei Kudo and Naozumi Ishimaru : NF-kB2 Controls the Migratory of Memory T cells to the Target Tissues in a Mouse Model of Sjogren's Syndorome by Regulating Expression of CXCR4., 11th International Congress of Autoimmunity, Lisbon, May 2018.
4.	Naozumi Ishimaru, Mie Kurosawa, Rieko Arakaki, Aya Ushio, otsuka kunihiro and Yasusei Kudo : Contributions of CXCL12 and its receptor to the T cell autoimmune response in a Sjögren's syndrome murine model., 14th International Symposium on Sjögren's Syndrome, Washington, D.C., Apr. 2018.

国内講演発表:

1.	新垣理恵子, 常松貴明, 木曽田暁, 石丸直澄, 牛尾綾 : Effect of inhalation exposure to acrbon nanotubes and titanium dioxide on alveolar macrophages, (キーワード) nanoparticle / alveolar macrophage
2.	松澤鎮史, 牛尾綾, 永尾瑠佳, 大塚邦紘, 俵宏彰, 常松貴明, 石丸直澄 : 新生仔の胸腺におけるオートファジーとシェーグレン症候群の関係性, 第113回日本病理学会総会, 2024年3月.
3.	永尾瑠佳, 山本安希子, 牛尾綾, 大塚邦紘, 松澤鎮史, 常松貴明, 石丸直澄 : シェーグレン症候群の病態形成におけるT細胞の共抑制性受容体役割の解析, 第113回日本病理学会総会, 2024年3月.
4.	牛尾綾, 大塚邦紘, 常松貴明, 高橋祐次, 菅野純, 石丸直澄 : The influence of multi-walled carbon nanotube for immune systems., 第113回日本病理学会総会, 2024年3月.
5.	俵宏彰, 常松貴明, 永尾瑠佳, 松澤鎮史, 大塚邦紘, 牛尾綾, 石丸直澄 : Borealin-Survivin複合体は頭頸部扁平上皮癌の分化を直接的に制御する, 第113回日本病理学会総会, 2024年3月.
6.	常松貴明, 𠮷川治孝, 永尾瑠, 松澤鎮史, 大塚邦紘, 牛尾綾, 石丸直澄 : がん特殊化リボソームの同定と機能解析, 第113回日本病理学会総会, 2024年3月.
7.	永尾瑠佳, 常松貴明, 松澤鎮史, 大塚邦紘, 牛尾綾, 石丸直澄 : 下顎骨腫瘍, 第143回日本病理学会中国四国支部学術集会, 2024年2月.
8.	松澤鎮史, 常松貴明, 永尾瑠佳, 大塚邦紘, 牛尾綾, 尾矢剛志, 石丸直澄 : 歯肉腫瘍, 日本病理学会中国四国支部学術集会(第143回スライドカンファレンス), 2024年2月.
9.	松澤鎮史, 牛尾綾, 永尾瑠佳, 大塚邦紘, 俵宏彰, 常松貴明, 石丸直澄 : 新生仔胸腺におけるT細胞の分化・成熟とオートファジーの関連についての検討, 2023年度感染・免疫クラスター・ミニリトリート, 2024年2月.
10.	MATSUZAWA Shigefumi, Aya Ushio, RUKA Nagao, TAWARA Hiroaki, Kunihiro Otsuka, Takaaki Tsunematsu and Naozumi Ishimaru : Investigation of the relationship between T cell differation and autophagy in the neonatal thymus., 第52回日本免疫学会総会・学術集会, Jan. 2024.
11.	RUKA Nagao, 山本安希子, Aya Ushio, Kunihiro Otsuka, TAWARA Hiroaki, MATSUZAWA Shigefumi, Kai Tamura, KAWAHITO Yuki, Takaaki Tsunematsu and Naozumi Ishimaru : Analysis of the suppression mechanism for activated T cells via co-inhibitory receptors in Sjogrens syndrome, 第52回日本免疫学会総会・学術集会, Jan. 2024.
12.	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.
13.	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.
14.	Takaaki Tsunematsu, RUKA Nagao, MATSUZAWA Shigefumi, Kunihiro Otsuka, Aya Ushio and Naozumi Ishimaru : The molecular mechanism of Cancer cell cannibalism and its significance in cancer progression, 第52回日本免疫学会総会・学術集会, Jan. 2024.
15.	Kunihiro Otsuka, Hiroyuki Kondo, Shin-ichi Tsukumo, Aya Ushio, Naozumi Ishimaru and Koji Yasutomo : CD153+ CD4+ T cells and CD30+ cells exacerbate the autoimmune pathology in salivary glands of Sjögren's syndrome, 第52回日本免疫学会学術集会, Jan. 2024.
16.	俵宏彰, 常松貴明, 大塚邦紘, 牛尾綾, 石丸直澄 : 口腔扁平上皮癌におけるSurvivinの核内蓄積がもたらす新たな機能, 第59回日本口腔組織培養学会総会・学術大会, 2023年11月.
17.	牛尾綾, 松田真美, 石丸直澄, 高浜洋介 : 機能的に異なる髄質胸腺上皮サブセットが中枢性自己寛容確立にもたらす相互作用, 第69回日本病理学会秋期特別総会, 2023年11月.
18.	牛尾綾 : 機能的に異なる髄質胸腺上皮サブセットが中枢性自己寛容確立にもたらす相互作用, 第69回日本病理学会秋期特別総会, 2023年11月.
19.	牛尾綾 : 機能的に異なる髄質胸腺上皮サブセットが中枢性自己寛容確立にもたらす相互作用, 第69回日本病理学会秋期特別総会, 2023年11月.
20.	松澤鎮史, 牛尾綾, 永尾瑠佳, 大塚邦紘, 俵宏彰, 常松貴明, 石丸直澄 : シェーグレン症候群と胸腺におけるT細胞の分化・成熟の関連についての検討, 第31回日本シェーグレン症候群学会学術集会, 2023年9月.
21.	大塚邦紘, 近藤博之, 九十九伸一, 牛尾綾, 永尾瑠佳, 青田桂子, 石丸直澄, 安友康二 : シングルセル解析を基盤としたシェーグレン症候群の病態解明, 第31回日本シェーグレン症候群学会学術集会, 2023年9月.
22.	牛尾綾, 松田真美, 石丸直澄, 高浜洋介 : 中枢性自己寛容確立に関わる機能的に異なる髄質胸腺上皮サブセットの相互作用, 第65回歯科基礎医学会学術大会, 2023年9月.
23.	俵宏彰, 常松貴明, 大塚邦紘, 牛尾綾, 石丸直澄 : 頭頚部扁平上皮癌における染色体パッセンジャー複合体非依存的なBorealin-Survivin相互作用がもたらす新たな機能, 第65回歯科基礎医学会学術大会, 2023年9月.
24.	TAWARA Hiroaki, Takaaki Tsunematsu, RUKA Nagao, MATSUZAWA Shigefumi, Aya Ushio, Kunihiro Otsuka and Naozumi Ishimaru : Novel role of nuclear Survivin in head and neck squamous carcinoma, 2023 Tokushima Bioscience Retreat, Sep. 2023.
25.	俵宏彰, 常松貴明, 永尾瑠佳, 松澤鎮史, 大塚邦紘, 牛尾綾, 石丸直澄 : 染色体パッセンジャー複合体構成因子Borealin-Survivin相互作用は頭頚部扁平上皮癌の代謝を制御する, 第34回日本臨床口腔病理学会総会・学術大会, 2023年8月.
26.	Aya Ushio : Developing the Career Path, Joint Symposium to Promote the Active Participation of Female Researchers, Aug. 2023.
27.	常松貴明, 俵宏彰, 佐藤真美, 福田一稀, 大塚邦紘, 牛尾綾, 石丸直澄 : 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, 2023年4月.
28.	俵宏彰, 常松貴明, 福田一稀, 永尾瑠佳, 佐藤真美, 大塚邦紘, 牛尾綾, 石丸直澄 : 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, 2023年4月.
29.	永尾瑠佳, 山本安希子, 大塚邦紘, 牛尾綾, 俵宏彰, 田中秀卓, 大塚邦紘, 常松貴明, 石丸直澄 : T細胞の共抑制性受容体を介したシェーグレン症候群の発症機序の解析, 第112回日本病理学会総会, 2023年4月.
30.	牛尾綾, 松田-Lennikov 真実, 大塚邦紘, 常松貴明, 石丸直澄, 高浜洋介 : 自己免疫疾患発症における多様性胸腺髄質上皮細胞の相乗的制御機構, 第112回日本病理学会総会, 2023年4月.
31.	大塚邦紘, 近藤博之, 九十九伸一, 新垣理恵子, 永尾瑠佳, 佐藤真美, 牛尾綾, 石丸直澄, 安友康二 : 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, 2023年4月.
32.	俵宏彰, 常松貴明, 永尾瑠佳, 福田一稀, 佐藤真美, 大塚邦紘, 牛尾綾, 石丸直澄 : 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, 2022年12月.
33.	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.
34.	常松貴明, 俵宏彰, 佐藤真美, 新垣理恵子, 大塚邦紘, 牛尾綾, 石丸直澄 : 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, 2022年9月.
35.	佐藤真美, 牛尾綾, 大塚邦紘, 常松貴明, 石丸直澄 : 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, 2022年9月.
36.	佐藤真美, 牛尾綾, 大塚邦紘, 常松貴明, 石丸直澄 : 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, 2022年8月.
37.	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.
38.	佐藤真美, 牛尾綾, 大塚邦紘, 常松貴明, 新垣理恵子, 石丸直澄 : 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, 2022年6月.
39.	大塚邦紘, 山田安希子, 齋藤雅子, 牛尾綾, 佐藤真美, 木曽田暁, 卲文華, 常松貴明, 工藤保誠, 新垣理恵子, 石丸直澄 : 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), 2021年8月.
40.	佐藤真美, 牛尾綾, 福田一稀, 俵宏彰, 大塚邦紘, 常松貴明, 新垣理恵子, 石丸直澄 : 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, 2021年6月.
41.	佐藤真美, 牛尾綾, 新垣理恵子, 俵宏彰, 常松貴明, 石丸直澄 : 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, 2021年3月.
42.	栗尾奈愛, 鎌田久美子, 横田美保, 山村佳子, 牛尾綾, 工藤保誠, 石丸直澄, 宮本洋二 : 上顎歯肉に発生した微小嚢胞性付属器癌の1例, 第38回日本口腔腫瘍学会総会・学術大会, 2020年1月.
43.	Aya Ushio, Rieko Arakaki, Akiko Yamada, Yasusei Kudo and Naozumi Ishimaru : Analysis of pulmonary lesions in a murlne model of sjogren's syndorome., Proceedings of the Japanese Society for Immunology, Dec. 2019.
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.	牛尾綾, 新垣理恵子, 工藤保誠, 石丸直澄 : 自己免疫疾患モデルにおける標的臓器常在型マクロファージの役割, 日本歯科基礎医学会誌, 2019年10月.
46.	Aya Ushio, Rieko Arakaki, Akiko Yamada, Yasusei Kudo and Naozumi Ishimaru : The new therapeutic strategy targeting chemokine in Sjogren's Syndorome., 日本RNAi研究会, Aug. 2019.
47.	木曽田暁, 卲文華, 牛尾綾, 佐藤真美, 新垣理恵子, 石丸直澄, 工藤保誠 : 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, 2019年7月.
48.	牛尾綾, 新垣理恵子, 工藤保誠, 石丸直澄 : シェーグレン症候群モデルマウスの唾液腺病態形成におけるマクロファージの役割, 第38回分子病理研究会, 2019年7月.
49.	牛尾綾, 新垣理恵子, 山田安希子, 工藤保誠, 石丸直澄 : シェーグレン症候群モデルマウスの標的組織マクロファージが病態形成に及ぼす影響, 第18回四国免疫フォーラム, 2019年6月.
50.	松倉春奈, 牛尾綾, 新垣理恵子, 工藤保誠, 石丸直澄 : シェーグレン症候群疾患モデルにおける胚病変の解析, 第108回日本病理学会総会, 2019年5月.
51.	牛尾綾, 新垣理恵子, 工藤保誠, 石丸直澄 : シェーグレン症候群病態形成におけるCCL22産生マクロファージの役割, 第108回日本病理学会総会, 2019年5月.
52.	Rieko Arakaki, Nakayama Shinichiro, Aya Ushio, Otsuka Kunihiro, Kisoda Satoshi, Takaaki Tsunematsu, Akiko Yamada, Yasusei Kudo and Naozumi Ishimaru : The role of the cleaved from IL-33 in pathogenesis of Sjogren's syndorome(SS), Proceedings of the Japanese Society for Immunology, Dec. 2018.
53.	Aya Ushio, Rieko Arakaki, Kunihiro Ohtsuka, Akiko Yamada, Yasusei Kudo and Naozumi Ishimaru : CCL22-producing macrophages promote T cell autoimmunity in the target organ of Sjogren's syndorome., Proceedings of the Japanese Society for Immunology, Dec. 2018.
54.	Kunihiro Ohtsuka, Akiko Yamada, Masako Saito, Aya Ushio, Satoru Kisoda, Takaaki Tsunematsu, Yasusei Kudo, Rieko Arakaki and Naozumi Ishimaru : A crucial role of follicular helper T cells in autoimmunity of a mouse model for Sjogren's syndorome., Proceedings of the Japanese Society for Immunology, Dec. 2018.
55.	大塚邦紘, 山田安希子, 齋藤雅子, 牛尾綾, 木曽田暁, 常松貴明, 工藤保誠, 新垣理恵子, 石丸直澄 : シェーグレン症候群疾患モデルの自己免疫病変における濾胞ヘルパーT細胞の役割, 日本シェーグレン症候群学会, 2018年9月.
56.	牛尾綾, 新垣理恵子, 大塚邦紘, 工藤保誠, 石丸直澄 : CCL22産生唾液腺マクロファージはシェーグレン症候群の病態に関与する, シェーグレン症候群学会, 2018年9月.
57.	大塚邦紘, 山田安希子, 齋藤雅子, 牛尾綾, 木曽田暁, 常松貴明, 工藤保誠, 新垣理恵子, 石丸直澄 : シェーグレン症候群疾患モデルの自己免疫病変における濾胞ヘルパーT細胞の役割, 日本歯科基礎医学会誌, 2018年9月.
58.	大塚邦紘, 山田安希子, 齋藤雅子, 牛尾綾, 木曽田暁, 常松貴明, 工藤保誠, 新垣理恵子, 石丸直澄 : Asc/2を介した濾胞ヘルパーT細胞分化異常が自己免疫疾患の病態形成に関与する．, 日本臨床口腔病理学会, 2018年8月.
59.	大塚邦紘, 山田安希子, 齋藤雅子, 牛尾綾, 木曽田暁, 常松貴明, 工藤保誠, 新垣理恵子, 石丸直澄 : シェーグレン症候群疾患モデルの自己免疫病変における濾胞ヘルパーT細胞の役割, 分子病理学研究会, 2018年7月.
60.	新垣理恵子, 牛尾綾, 大塚邦紘, 工藤保誠, 石丸直澄 : 全身吸入暴露による多層化カーボンナノチューブの肺胞マクロファージへの影響, 日本病理学会会誌, Vol.107, 2018年6月.
61.	中山慎一朗, 新垣理恵子, 牛尾綾, 大塚邦紘, 常松貴明, 工藤保誠, 石丸直澄 : シェーグレン症候群モデルマウス唾液腺におけるIL-33の発現とその役割, 日本病理学会会誌, Vol.107, 2018年6月.
62.	西條早紀, 大塚邦紘, 常松貴明, 大塚邦紘, 牛尾綾, 新垣理恵子, 工藤保誠, 石丸直澄 : Emi1の過剰発現による人工口腔癌幹細胞の作成, 日本病理学会会誌, Vol.107, 2018年6月.
63.	沼田雪乃, 大塚邦紘, 山田安希子, 牛尾綾, 常松貴明, 工藤保誠, 新垣理恵子, 石丸直澄 : シェーグレン症候群疾患モデルにおけるNotchシグナルの役割, 日本病理学会会誌, Vol.107, 2018年6月.
64.	大塚邦紘, 山田安希子, 齋藤雅子, 牛尾綾, 常松貴明, 工藤保誠, 新垣理恵子, 石丸直澄 : シェーグレン症候群疾患モデルの自己免疫病変における濾胞ヘルパーT細胞の役割, 日本病理学会会誌, Vol.107, 2018年6月.
65.	牛尾綾, 新垣理恵子, 山田安希子, 大塚邦紘, 工藤保誠, 石丸直澄 : CCL22-producing resident macrophages enhancesnautoimmune lesions in a mouse model of Sjogren's syndorome., 日本免疫学会総会·学術集会記録, Vol.46, 119, 2017年12月.
66.	大塚邦紘, 山田安希子, 牛尾綾, 黒澤実愛, 新垣理恵子, 工藤保誠, 石丸直澄 : Analysis of follicular helper T cells in a mouse model for Sjogren's syndorome., 日本免疫学会総会·学術集会記録, Vol.46, 81, 2017年12月.
67.	大塚邦紘, 山田安希子, 齋藤雅子, 牛尾綾, 鯨岡聡子, 黒澤実愛, 常松貴明, 新垣理恵子, 工藤保誠, 石丸直澄 : シェーグレン症候群疾患モデルにおける胚中心反応の解析, 第28回日本臨床口腔病理学会, Vol.28, 2017年8月.

その他・研究会:

1.	林亜門, 清水朱里, 中西美緒, 山内加奈, 佐藤真美, 邵文華, 木曽田暁, 福井仁美, 木野倫子, 牛尾綾, 山田安希子, 常松貴明, 新垣理恵子, 工藤保誠, 石丸直澄 : 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), 2020年2月.

科学研究費補助金 (KAKEN Grants Database @ NII.ac.jp)

新生仔期胸腺におけるT細胞分化が自己免疫疾患の発症に与える影響 (研究課題/領域番号: 24K19862 )
免疫難病における自己抗体産生機構の解明と多角的臨床応用 (研究課題/領域番号: 23K18361 )
免疫チューニング分子を基盤とした自己免疫疾患の新たな病因論の確立と治療戦略 (研究課題/領域番号: 23H00438 )
性ホルモンと自然免疫を介したシェーグレン症候群の新たな病因論の構築 (研究課題/領域番号: 19K18965 )
臓器間コミュニケーションを介した自己免疫疾患発症機序の解明 (研究課題/領域番号: 19H01070 )
自然免疫を介した自己免疫疾患病態機序の解明～シェーグレン症候群の新たな病因論～ (研究課題/領域番号: 18H06279 )
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講師 : 牛尾綾