Tokushima University / Educator and Researcher Directory --- Ushio, Aya

Field of Study

○	Oral Pathology

Subject of Study

○	シェーグレン症候群の病態解明 (Sjögren's syndrome, Autoimmune disease, model mice)

Book / Paper

Book:

1.	Takaaki Tsunematsu, 俵宏彰, Kunihiro Otsuka, Aya Ushio and Naozumi Ishimaru : 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, Nov. 2022.
2.	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.	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. (Summary) 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. (Keyword) Humans / Survivin / Centromere / Chromosomal Proteins, Non-Histone / Cell Cycle Proteins / Mitosis / Phosphorylation / Aurora Kinase B / Carcinoma, Squamous Cell / Lactates (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbrc.2024.149741 (Link to Search Site for Scientific Articles) ● 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. (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.	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. (Summary) 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. (Tokushima University Institutional Repository) ● Metadata: 116455 (Link to Publication Site) ● Publication site (DOI): 10.1084/jem.20201904 (Link to Search Site for Scientific Articles) ● 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 (Tokushima University Institutional Repository: 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. (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)
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. (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)
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. (Summary) 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. (Tokushima University Institutional Repository) ● Metadata: 113526 (Link to Publication Site) ● Publication site (DOI): 10.3389/fimmu.2018.02594 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30467506 ● Summary page in Scopus @ Elsevier: 2-s2.0-85056303968 (Tokushima University Institutional Repository: 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. (Summary) 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. (Tokushima University Institutional Repository) ● Metadata: 113371 (Link to Publication Site) ● Publication site (DOI): 10.1371/journal.pone.0205702 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30372450 ● Summary page in Scopus @ Elsevier: 2-s2.0-85055616395 (Tokushima University Institutional Repository: 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. (Summary) 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. (Tokushima University Institutional Repository) ● Metadata: 111713 (Link to Publication Site) ● Publication site (DOI): 10.3390/ijms18061209 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28587293 ● Search Scopus @ Elsevier (PMID): 28587293 ● Search Scopus @ Elsevier (DOI): 10.3390/ijms18061209 (Tokushima University Institutional Repository: 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. (Summary) 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. (Tokushima University Institutional Repository) ● Metadata: 111726 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.oraloncology.2017.04.003 (Link to Search Site for Scientific Articles) ● 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 (Tokushima University Institutional Repository: 111726, DOI: 10.1016/j.oraloncology.2017.04.003, PubMed: 28559020)

Proceeding of International Conference:

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.

Proceeding of Domestic Conference:

1.	Rieko Arakaki, Takaaki Tsunematsu, Satoru Kisoda, Naozumi Ishimaru and Aya Ushio : Effect of inhalation exposure to acrbon nanotubes and titanium dioxide on alveolar macrophages, (Keyword) nanoparticle / alveolar macrophage
2.	MATSUZAWA Shigefumi, Aya Ushio, RUKA Nagao, Kunihiro Otsuka, TAWARA Hiroaki, Takaaki Tsunematsu and Naozumi Ishimaru : 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, Mar. 2024.
3.	RUKA Nagao, 山本安希子, Aya Ushio, Kunihiro Otsuka, MATSUZAWA Shigefumi, Takaaki Tsunematsu and Naozumi Ishimaru : 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, Mar. 2024.
4.	Aya Ushio, Kunihiro Otsuka, Takaaki Tsunematsu, 高橋祐次, 菅野純 and Naozumi Ishimaru : The influence of multi-walled carbon nanotube for immune systems., 第113回日本病理学会総会, Mar. 2024.
5.	Hiroaki Tawara, Takaaki Tsunematsu, RUKA Nagao, MATSUZAWA Shigefumi, Kunihiro Otsuka, Aya Ushio and Naozumi Ishimaru : 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, Mar. 2024.
6.	Takaaki Tsunematsu, Harunori Yoshikawa, RUKA Nagao, MATSUZAWA Shigefumi, Kunihiro Otsuka, Aya Ushio and Naozumi Ishimaru : 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, Mar. 2024.
7.	RUKA Nagao, Takaaki Tsunematsu, MATSUZAWA Shigefumi, Kunihiro Otsuka, Aya Ushio and Naozumi Ishimaru : 下顎骨腫瘍, 第143回日本病理学会中国四国支部学術集会, Feb. 2024.
8.	MATSUZAWA Shigefumi, Takaaki Tsunematsu, RUKA Nagao, Kunihiro Otsuka, Aya Ushio, Takeshi Oya and Naozumi Ishimaru : 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), Feb. 2024.
9.	MATSUZAWA Shigefumi, Aya Ushio, RUKA Nagao, Kunihiro Otsuka, TAWARA Hiroaki, Takaaki Tsunematsu and Naozumi Ishimaru : 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, Feb. 2024.
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.	Hiroaki Tawara, Takaaki Tsunematsu, Kunihiro Otsuka, Aya Ushio and Naozumi Ishimaru : 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, Nov. 2023.
17.	Aya Ushio, 松田真美, Naozumi Ishimaru and Yousuke Takahama : 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, Nov. 2023.
18.	Aya Ushio : Interplay between functionally distinct medullary thymic epithelial subsets for central self-tolerance, 第69回日本病理学会秋期特別総会, Nov. 2023.
19.	Aya Ushio : Interplay between functionally distinct medullary thymic epithelial subsets for central self-tolerance, 第69回日本病理学会秋期特別総会, Nov. 2023.
20.	MATSUZAWA Shigefumi, Aya Ushio, RUKA Nagao, Kunihiro Otsuka, TAWARA Hiroaki, Takaaki Tsunematsu and Naozumi Ishimaru : 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, Sep. 2023.
21.	Kunihiro Otsuka, Hiroyuki Kondo, Shin-ichi Tsukumo, Aya Ushio, RUKA Nagao, Keiko Aota, Naozumi Ishimaru and Koji Yasutomo : 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, Sep. 2023.
22.	Aya Ushio, 松田真美, Naozumi Ishimaru and Yousuke Takahama : 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, Sep. 2023.
23.	TAWARA Hiroaki, Takaaki Tsunematsu, Kunihiro Otsuka, Aya Ushio and Naozumi Ishimaru : 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, Sep. 2023.
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.	TAWARA Hiroaki, Takaaki Tsunematsu, RUKA Nagao, MATSUZAWA Shigefumi, 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, Aug. 2023.
26.	Aya Ushio : Developing the Career Path, Joint Symposium to Promote the Active Participation of Female Researchers, Aug. 2023.
27.	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.
28.	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.
29.	RUKA Nagao, 山本安希子, Kunihiro Otsuka, Aya Ushio, TAWARA Hiroaki, TANAKA Hidetaka, Kunihiro Otsuka, Takaaki Tsunematsu and Naozumi Ishimaru : 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, Apr. 2023.
30.	Aya Ushio, 松田-Lennikov 真実, Kunihiro Otsuka, Takaaki Tsunematsu, Naozumi Ishimaru and Yousuke Takahama : 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, Apr. 2023.
31.	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.
32.	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.
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.	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.
35.	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.
36.	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.
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.	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.
39.	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.
40.	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.
41.	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.
42.	Naito Kurio, Kumiko Kamada, 横田美保, Yoshiko Yamamura, Aya Ushio, Yasusei Kudo, Naozumi Ishimaru and Youji Miyamoto : 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, Jan. 2020.
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.	Aya Ushio, Rieko Arakaki, Yasusei Kudo and Naozumi Ishimaru : 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, Japanese Journal of Oral Biology, Oct. 2019.
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.	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.
48.	Aya Ushio, Rieko Arakaki, Yasusei Kudo and Naozumi Ishimaru : 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, Jul. 2019.
49.	Aya Ushio, Rieko Arakaki, Akiko Yamada, Yasusei Kudo and Naozumi Ishimaru : 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, Jun. 2019.
50.	Haruna Matsukura, Aya Ushio, Rieko Arakaki, Yasusei Kudo and Naozumi Ishimaru : 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, May 2019.
51.	Aya Ushio, Rieko Arakaki, Yasusei Kudo and Naozumi Ishimaru : 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, May 2019.
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.	Kunihiro Ohtsuka, Akiko Yamada, Masako Saito, Aya Ushio, Satoru Kisoda, Takaaki Tsunematsu, Yasusei Kudo, Rieko Arakaki and Naozumi Ishimaru : 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, Sep. 2018.
56.	Aya Ushio, Rieko Arakaki, Kunihiro Ohtsuka, Yasusei Kudo and Naozumi Ishimaru : 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, Sep. 2018.
57.	Kunihiro Ohtsuka, Akiko Yamada, Masako Saito, Aya Ushio, Satoru Kisoda, Takaaki Tsunematsu, Yasusei Kudo, Rieko Arakaki and Naozumi Ishimaru : 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, Japanese Journal of Oral Biology, Sep. 2018.
58.	Kunihiro Ohtsuka, Akiko Yamada, Masako Saito, Aya Ushio, Satoru Kisoda, Takaaki Tsunematsu, Yasusei Kudo, Rieko Arakaki and Naozumi Ishimaru : 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, Aug. 2018.
59.	Kunihiro Ohtsuka, Akiko Yamada, Masako Saito, Aya Ushio, Satoru Kisoda, Takaaki Tsunematsu, Yasusei Kudo, Rieko Arakaki and Naozumi Ishimaru : 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, Jul. 2018.
60.	Rieko Arakaki, Aya Ushio, Kunihiro Ohtsuka, Yasusei Kudo and Naozumi Ishimaru : 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, Proceedings of the Japanese Society of Pathology, Vol.107, Jun. 2018.
61.	Shinichiroh Nakayama, Rieko Arakaki, Aya Ushio, Kunihiro Ohtsuka, Takaaki Tsunematsu, Yasusei Kudo and Naozumi Ishimaru : 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, Proceedings of the Japanese Society of Pathology, Vol.107, Jun. 2018.
62.	Saki Saijoh, Kunihiro Ohtsuka, Takaaki Tsunematsu, Kunihiro Ohtsuka, Aya Ushio, Rieko Arakaki, Yasusei Kudo and Naozumi Ishimaru : Emi1の過剰発現による人工口腔癌幹細胞の作成, Proceedings of the Japanese Society of Pathology, Vol.107, Jun. 2018.
63.	Yukino Numata, Kunihiro Ohtsuka, Akiko Yamada, Aya Ushio, Takaaki Tsunematsu, Yasusei Kudo, Rieko Arakaki and Naozumi Ishimaru : 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, Proceedings of the Japanese Society of Pathology, Vol.107, Jun. 2018.
64.	Kunihiro Ohtsuka, Akiko Yamada, Masako Saito, Aya Ushio, Takaaki Tsunematsu, Yasusei Kudo, Rieko Arakaki and Naozumi Ishimaru : 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, Proceedings of the Japanese Society of Pathology, Vol.107, Jun. 2018.
65.	Aya Ushio, Rieko Arakaki, Akiko Yamada, Kunihiro Ohtsuka, Yasusei Kudo and Naozumi Ishimaru : CCL22-producing resident macrophages enhancesnautoimmune lesions in a mouse model of Sjogren's syndorome., Proceedings of the Japanese Society for Immunology, Vol.46, 119, Dec. 2017.
66.	Kunihiro Ohtsuka, Akiko Yamada, Aya Ushio, Mie Kurosawa, Rieko Arakaki, Yasusei Kudo and Naozumi Ishimaru : Analysis of follicular helper T cells in a mouse model for Sjogren's syndorome., Proceedings of the Japanese Society for Immunology, Vol.46, 81, Dec. 2017.
67.	Kunihiro Ohtsuka, Akiko Yamada, Masako Saito, Aya Ushio, Satoko Kujiraoka, Mie Kurosawa, Takaaki Tsunematsu, Rieko Arakaki, Yasusei Kudo and Naozumi Ishimaru : 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, Aug. 2017.

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.

Grants-in-Aid for Scientific Research (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 (Project/Area Number: 24K19862 )
Clinical application based on the molecular mechanism of autoantibody production in autoimmunity (Project/Area Number: 23K18361 )
Novel pathogenesis and therapeutic strategy of autoimmunity based on immune-tuning molecules (Project/Area Number: 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 (Project/Area Number: 19K18965 )
Analysis of Pathogenesis of Autoimmunity through Communication between Organs (Project/Area Number: 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～ (Project/Area Number: 18H06279 )
Search by Researcher Number (40823836)

Associate Professor : Ushio, Aya

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Grants-in-Aid for Scientific Research (KAKEN Grants Database @ NII.ac.jp)