徳島大学 / 教育研究者総覧 --- 大塚邦紘

個人のホームページ

https://researchmap.jp/tsukahiro (researchmap)

https://orcid.org/0000-0002-3546-8143 (ORCID)

専門分野

○	病理学 (Pathology), 免疫学 (Immunology)

研究テーマ

○	免疫病理学 (シェーグレン症候群 (Sjögren's syndrome), 自己免疫疾患, 特発性肺線維症, 非標識イメージング)

著書・論文

著書:

1.	大塚邦紘, 常松貴明, 石丸直澄 : シェーグレン症候群の病理診断, 日本病理学会,
2.	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.
3.	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 (徳島大学機関リポジトリ) ● Metadata: 119377 (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 (徳島大学機関リポジトリ: 119377, DOI: 10.1016/j.bbrc.2024.149741, PubMed: 38471204)
2.	Shogo Miyamura, Ryo Oe, Takuya Nakahara, Hidenori Koresawa, Shota Okada, Shuji Taue, Yu Tokizane, Takeo Minamikawa, Kunihiro Otsuka, Ayuko Sakane, Takuya Sasaki, Koji Yasutomo, Taira Kajisa and Takeshi Yasui : Rapid, high-sensitivity detection of biomolecules using dual-comb biosensing, Scientific Reports, Vol.13, 14541, 2023. (要約) Rapid, sensitive detection of biomolecules is important for biosensing of infectious pathogens as well as biomarkers and pollutants. For example, biosensing of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is still strongly required for the fight against coronavirus disease 2019 (COVID-19) pandemic. Here, we aim to achieve the rapid and sensitive detection of SARS-CoV-2 nucleocapsid protein antigen by enhancing the performance of optical biosensing based on optical frequency combs (OFC). The virus-concentration-dependent optical spectrum shift produced by antigen-antibody interactions is transformed into a photonic radio-frequency (RF) shift by a frequency conversion between the optical and RF regions in the OFC, facilitating rapid and sensitive detection with well-established electrical frequency measurements. Furthermore, active-dummy temperature-drift compensation with a dual-comb configuration enables the very small change in the virus-concentration-dependent signal to be extracted from the large, variable background signal caused by temperature disturbance. The achieved performance of dual-comb biosensing will greatly enhance the applicability of biosensors to viruses, biomarkers, environmental hormones, and so on. (キーワード) Humans / COVID-19 / SARS-CoV-2 / COVID-19 Testing / Biosensing Techniques / Viruses / Antigens, Viral (出版サイトへのリンク) ● Publication site (DOI): 10.1038/s41598-023-41436-3 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37752134 ● Search Scopus @ Elsevier (PMID): 37752134 ● Search Scopus @ Elsevier (DOI): 10.1038/s41598-023-41436-3 (DOI: 10.1038/s41598-023-41436-3, PubMed: 37752134)
3.	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)
4.	Thiranut Jaroonwitchawan, Hideki Arimochi, Yuki Sasaki, Chieko Ishifune, Hiroyuki Kondo, Kunihiro Otsuka, Shin-ichi Tsukumo and Koji Yasutomo : Stimulation of the farnesoid X receptor promotes M2 macrophage polarization., Frontiers in Immunology, Vol.14, 2023. (要約) This skewed polarization towards M2 macrophages by an FXR agonist was accompanied by increased expression of signaling molecules related to the retinoic acid receptor. Inhibition of the retinoic acid receptor suppressed FXR agonist-mediated M2 macrophage polarization, indicating that this polarization was, at least, partly dependent on the retinoic acid receptor pathway. These data demonstrate that FXR has a role in polarization toward M2 macrophages and suggest a possible therapeutic potential of FXR agonists in M2 macrophage-related conditions. (キーワード) Receptors, Cytoplasmic and Nuclear (徳島大学機関リポジトリ) ● Metadata: 118291 (出版サイトへのリンク) ● Publication site (DOI): 10.3389/fimmu.2023.1065790 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36776885 ● Search Scopus @ Elsevier (PMID): 36776885 ● Search Scopus @ Elsevier (DOI): 10.3389/fimmu.2023.1065790 (徳島大学機関リポジトリ: 118291, DOI: 10.3389/fimmu.2023.1065790, PubMed: 36776885)
5.	Taira Kajisa, Taka-aki Yano, Hidenori Koresawa, Kunihiro Otsuka, Ayuko Sakane, Takuya Sasaki, Koji Yasutomo and Takeshi Yasui : Highly sensitive detection of nucleocapsid protein from SARS-CoV-2 using a near-infrared surface plasmon resonance sensing system, Optics Continuum, Vol.11, No.1, 2336-2346, 2022. (出版サイトへのリンク) ● Publication site (DOI): 10.1364/OPTCON.472486 (文献検索サイトへのリンク) ● Search Scopus @ Elsevier (DOI): 10.1364/OPTCON.472486 (DOI: 10.1364/OPTCON.472486)
6.	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. (要約) 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. (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.ajpath.2022.07.009 (文献検索サイトへのリンク) ● 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)
7.	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. (要約) 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. (キーワード) Autoantigens / 自己免疫 (autoimmunity) / Herpesvirus 4, Human / Humans / シェーグレン症候群 (Sjögren's syndrome) / Virus Diseases (徳島大学機関リポジトリ) ● Metadata: 117727 (出版サイトへのリンク) ● Publication site (DOI): 10.3390/v14071474 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35891453 ● Summary page in Scopus @ Elsevier: 2-s2.0-85133687255 (徳島大学機関リポジトリ: 117727, DOI: 10.3390/v14071474, PubMed: 35891453, Elsevier: Scopus)
8.	Hiroyuki Kondo, Takahiro Kageyama, Shigeru Tanaka, Kunihiro Otsuka, Shin-ichi Tsukumo, Yoichi Mashimo, Yoshihiro Onouchi, Hiroshi Nakajima and Koji Yasutomo : Markers of Memory CD8 T Cells Depicting the Effect of the BNT162b2 mRNA COVID-19 Vaccine in Japan., Frontiers in Immunology, Vol.13, 2022. (要約) BNT162b2, a nucleoside-modified mRNA vaccine for SARS-CoV-2 spike glycoprotein (S), provides approximately 95% efficacy for preventing COVID-19. However, it remains unclear how effectively memory CD8+ T cells are generated and which genetic and environmental factors affect the generation and function of memory CD8+ T cells elicited by this vaccine. Here, we investigated the frequency and functions of memory CD8+ T cells 3 weeks after the second vaccination in the Japanese population. Using a peptide-MHC pentamer, we detected an increased number of memory CD8+ T cells together with increased serum anti-S protein antibody in females compared with that in males, but the frequency of pentamer-positive cells was not positively correlated with antibody titers. Memory precursor effector cells (KLRG1-CD127+) among both CD8+ cells and pentamer+ cells and effector cells (CD38-HLA-DR+) among pentamer+ cells were more abundant in females than in males. Upon S protein-mediated stimulation of T cells, the intensity of CD107a and granzyme B expression was increased in females compared with that in males, indicating stronger memory CD8+ T cell responses in females than in males. Our studies showed that the BNT162b2 vaccine elicits increased memory CD8+ T cell proliferation and secondary CTL responses in females compared with those in males in the Japanese population. These findings provide an important basis for the distinct sex difference in cellular immune responses to mRNA vaccination and suggest that memory precursor effector cells can be one of markers to evaluate and boost cellular immunity induced by BNT162b2. (徳島大学機関リポジトリ) ● Metadata: 117815 (出版サイトへのリンク) ● Publication site (DOI): 10.3389/fimmu.2022.836923 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35572546 ● Search Scopus @ Elsevier (PMID): 35572546 ● Search Scopus @ Elsevier (DOI): 10.3389/fimmu.2022.836923 (徳島大学機関リポジトリ: 117815, DOI: 10.3389/fimmu.2022.836923, PubMed: 35572546)
9.	Yuki Sasaki, Hideki Arimochi, Kunihiro Otsuka, Hiroyuki Kondo, Shin-ichi Tsukumo and Koji Yasutomo : Blockade of the CXCR3/CXCL10 axis ameliorates inflammation caused by immunoproteasome dysfunction., JCI Insight, Vol.7, No.7, 2022. (要約) Immunoproteasomes regulate the degradation of ubiquitin-coupled proteins and generate peptides that are preferentially presented by MHC class I. Mutations in immunoproteasome subunits lead to immunoproteasome dysfunction, which causes proteasome-associated autoinflammatory syndromes (PRAAS) characterized by nodular erythema and partial lipodystrophy. It remains unclear, however, how immunoproteasome dysfunction leads to inflammatory symptoms. Here, we established mice harboring a mutation in Psmb8 (Psmb8-KI mice) and addressed this question. Psmb8-KI mice showed higher susceptibility to imiquimod-induced skin inflammation (IMS). Blockade of IL-6 or TNF-α partially suppressed IMS in both control and Psmb8-KI mice, but there was still more residual inflammation in the Psmb8-KI mice than in the control mice. DNA microarray analysis showed that treatment of J774 cells with proteasome inhibitors increased the expression of the Cxcl9 and Cxcl10 genes. Deficiency in Cxcr3, the gene encoding the receptor of CXCL9 and CXCL10, in control mice did not change IMS susceptibility, while deficiency in Cxcr3 in Psmb8-KI mice ameliorated IMS. Taken together, these findings demonstrate that this mutation in Psmb8 leads to hyperactivation of the CXCR3 pathway, which is responsible for the increased susceptibility of Psmb8-KI mice to IMS. These data suggest the CXCR3/CXCL10 axis as a new molecular target for treating PRAAS. (徳島大学機関リポジトリ) ● Metadata: 117226 (出版サイトへのリンク) ● Publication site (DOI): 10.1172/jci.insight.152681 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35393946 ● Search Scopus @ Elsevier (PMID): 35393946 ● Search Scopus @ Elsevier (DOI): 10.1172/jci.insight.152681 (徳島大学機関リポジトリ: 117226, DOI: 10.1172/jci.insight.152681, PubMed: 35393946)
10.	Taka-aki Yano, Taira Kajisa, Masayuki Ono, Yoshiya Miyasaka, Yuichi Hasegawa, Atsushi Saito, Kunihiro Otsuka, Ayuko Sakane, Takuya Sasaki, Koji Yasutomo, Rina Hamajima, Yuta Kanai, Takeshi Kobayashi, Yoshiharu Matsuura, Makoto Itonaga and Takeshi Yasui : Ultrasensitive detection of SARS-CoV-2 nucleocapsid protein using large gold nanoparticle-enhanced surface plasmon resonance., Scientific Reports, Vol.12, No.1, 1060, 2022. (要約) The COVID-19 pandemic has created urgent demand for rapid detection of the SARS-CoV-2 coronavirus. Herein, we report highly sensitive detection of SARS-CoV-2 nucleocapsid protein (N protein) using nanoparticle-enhanced surface plasmon resonance (SPR) techniques. A crucial plasmonic role in significantly enhancing the limit of detection (LOD) is revealed for exceptionally large gold nanoparticles (AuNPs) with diameters of hundreds of nm. SPR enhanced by these large nanoparticles lowered the LOD of SARS-CoV-2 N protein to 85 fM, resulting in the highest SPR detection sensitivity ever obtained for SARS-CoV-2 N protein. (キーワード) Coronavirus Nucleocapsid Proteins / Gold / Metal Nanoparticles / Phosphoproteins / SARS-CoV-2 / Surface Plasmon Resonance (徳島大学機関リポジトリ) ● Metadata: 117264 (出版サイトへのリンク) ● Publication site (DOI): 10.1038/s41598-022-05036-x (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35058513 ● Search Scopus @ Elsevier (PMID): 35058513 ● Search Scopus @ Elsevier (DOI): 10.1038/s41598-022-05036-x (徳島大学機関リポジトリ: 117264, DOI: 10.1038/s41598-022-05036-x, PubMed: 35058513)
11.	Michittra Boonchan, Hideki Arimochi, Kunihiro Otsuka, Tomoko Kobayashi, Hisanori Uehara, Thiranut Jaroonwitchawan, Yuki Sasaki, Shin-ichi Tsukumo and Koji Yasutomo : Necroptosis protects against exacerbation of acute pancreatitis., Cell Death & Disease, Vol.12, No.6, 601, 2021. (要約) mice exhibit weight loss, edematous pancreatitis, necrotizing pancreatitis, and acinar cell dedifferentiation in response to tissue damage. Genetic deletion of Mlkl resulted in downregulation of the antiapoptotic genes Bclxl and Cflar in association with increases in the numbers of apoptotic cells, as detected by TUNEL assay. These findings suggest that RIPK3 and MLKL-mediated necroptosis exerts protective effects in AP and caution against the use of necroptosis inhibitors for AP treatment. (徳島大学機関リポジトリ) ● Metadata: 116381 (出版サイトへのリンク) ● Publication site (DOI): 10.1038/s41419-021-03847-w (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34112763 ● Search Scopus @ Elsevier (PMID): 34112763 ● Search Scopus @ Elsevier (DOI): 10.1038/s41419-021-03847-w (徳島大学機関リポジトリ: 116381, DOI: 10.1038/s41419-021-03847-w, PubMed: 34112763)
12.	Yuki Sasaki, Kunihiro Otsuka, Hideki Arimochi, Shin-ichi Tsukumo and Koji Yasutomo : Distinct Roles of IL-1 and IL-18 in NLRC4-Induced Autoinflammation., Frontiers in Immunology, Vol.11, 591713, 2020. (要約) The NLRC4 inflammasome assembles in response to detection of bacterial invasion, and NLRC4 activation leads to the production of IL-1 and IL-18 together with pyroptosis-mediated cell death. Missense activating mutations in cause autoinflammatory disorders whose symptoms are distinctly dependent on the site of mutation and other aspects of the genetic background. To determine the involvement of IL-1 and IL-18 in the inflammation induced by mutation, we depleted IL-1 , IL-18, or both cytokines in Nlrc4-transgenic mice in which mutant is expressed under the MHC class II promoter (Nlrc4-H443P-Tg mice). The deletion of the or gene in Nlrc4-H443P-Tg mice reduced the neutrophil numbers in the spleen, and mice with deletion of both genes had an equivalent number of neutrophils compared to wild-type mice. Deletion of ameliorated but did not eliminate bone marrow hyperplasia, while mice deficient in showed no bone marrow hyperplasia. In contrast, tail bone deformity remained in the presence of deficiency, but deficiency completely abolished bone deformity. The decreased bone density in Nlrc4-H443P-Tg mice was counteracted by but not deficiency. Our results demonstrate the distinct effects of IL-1 and IL-18 on NLRC4-induced inflammation among tissues, which suggests that blockers for each cytokine should be utilized depending on the site of inflammation. (徳島大学機関リポジトリ) ● Metadata: 116191 (出版サイトへのリンク) ● Publication site (DOI): 10.3389/fimmu.2020.591713 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33178225 ● Summary page in Scopus @ Elsevier: 2-s2.0-85094604314 (徳島大学機関リポジトリ: 116191, DOI: 10.3389/fimmu.2020.591713, PubMed: 33178225, Elsevier: Scopus)
13.	Aya Miyazaki, Asuna Sugimoto, Keigo Yoshizaki, Keita Kawarabayashi, Kokoro Iwata, Rika Kurogohshi, Takamasa Kitamura, Kunihiro Otsuka, Tomokazu Hasegawa, Yuki Akazawa, Satoshi Fukumoto, Naozumi Ishimaru and Tsutomu Iwamoto : Coordination of WNT signaling and ciliogenesis during odontogenesis by piezo type mechanosensitive ion channel component 1, Scientific Reports, Vol.9, No.1, 14762, 2019. (要約) Signal transmission from the mechanical forces to the various intracellular activities is a fundamental process during tissue development. Despite their critical role, the mechanism of mechanical forces in the biological process is poorly understood. In this study, we demonstrated that in the response to hydrostatic pressure (HP), the piezo type mechanosensitive ion channel component 1 (PIEZO1) is a primary mechanosensing receptor for odontoblast differentiation through coordination of the WNT expression and ciliogenesis. In stem cells from human exfoliated deciduous teeth (SHED), HP significantly promoted calcium deposition as well as the expression of odontogenic marker genes, PANX3 and DSPP, and WNT related-genes including WNT5b and WNT16, whereas HP inhibited cell proliferation and enhanced primary cilia expression. WNT signaling inhibitor XAV939 and primary cilia inhibitor chloral hydrate blocked the HP-induced calcium deposition. The PIEZO1 activator Yoda1 inhibited cell proliferation but induced ciliogenesis and WNT16 expression. Interestingly, HP and Yoda1 promoted nuclear translocation of RUNX2, whereas siRNA-mediated silencing of PIEZO1 decreased HP-induced nuclear translocation of RUNX2. Taken together, these results suggest that PIEZO1 functions as a mechanotransducer that connects HP signal to the intracellular signalings during odontoblast differentiation. (徳島大学機関リポジトリ) ● Metadata: 114667 (出版サイトへのリンク) ● Publication site (DOI): 10.1038/s41598-019-51381-9 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31611621 ● Search Scopus @ Elsevier (PMID): 31611621 ● Search Scopus @ Elsevier (DOI): 10.1038/s41598-019-51381-9 (徳島大学機関リポジトリ: 114667, DOI: 10.1038/s41598-019-51381-9, PubMed: 31611621)
14.	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)
15.	Rieko Arakaki, Aya Ushio, Kunihiro Otsuka, Yasusei Kudo and Naozumi Ishimaru : A novel method for measuring small amounts of saliva in mice, Oral Science International, Vol.16, No.3, 178-180, 2019. (出版サイトへのリンク) ● Publication site (DOI): 10.1002/osi2.1013 (文献検索サイトへのリンク) ● Summary page in Scopus @ Elsevier: 2-s2.0-85065772725 (DOI: 10.1002/osi2.1013, Elsevier: Scopus)
16.	牛尾綾, Kunihiro Otsuka, Rieko Arakaki, Yasusei Kudo and Naozumi Ishimaru : CCL22 and autoimmune diseases, Clinical Immunology & Allergology, Vol.71, No.5, 520-526, 2019. (キーワード) C-C motif chemokine 22 (CCL22) / autoimmunity / macrophage / T-cell / Sjogren's syndrome (SS) (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1520010378554631296 (CiNii: 1520010378554631296)

学術論文(紀要・その他):

1.	鈴木昭浩, 大塚邦紘, 髙成広起, 永松謙太郎, 白井昭博 : 次世代光による細胞光応答の解明, LED総合フォーラム 2020 in 徳島論文集, Vol.P-17, 105-106, 2020年.

総説・解説:

1.	大塚邦紘, 安友康二 : 新規動物モデルを用いた肺線維症の発症機構の解明, 医学のあゆみ, Vol.283, No.1, 41-46, 2022年10月. (出版サイトへのリンク) ● Publication site (DOI): 10.32118/ayu2830141 (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1390018218936931968 ● Search Scopus @ Elsevier (DOI): 10.32118/ayu2830141 (DOI: 10.32118/ayu2830141, CiNii: 1390018218936931968)
2.	大塚邦紘, 安友康二 : 特発性肺線維症の病態におけるネクロプトーシス, 臨床免疫·アレルギー科, Vol.74, No.2, 192-198, 2020年8月. (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1520010380775998720 (CiNii: 1520010380775998720)
3.	大塚邦紘, 石丸直澄 : シェーグレン症候群における濾胞ヘルパーT細胞の役割 (特集濾胞ヘルパーT細胞と疾患), 臨床免疫·アレルギー科, Vol.73, No.3, 241-248, 2020年3月. (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1521699230266946688 (CiNii: 1521699230266946688)
4.	大塚邦紘, 安友康二 : ヒト免疫疾患の疾患遺伝子解析からのアプローチ家族性肺線維症の原因遺伝子同定研究から肺線維化の病態を探る, 炎症と免疫, Vol.28, No.6, 454-459, 2020年.
5.	大塚邦紘, 安友康二 : 遺伝・ゲノム学特発性肺線維症と遺伝子変異, 医学のあゆみ, Vol.275, No.9, 988-989, 2020年.

国際会議:

1.	Kunihiro Otsuka, Hiroyuki Kondo, Shin-ichi Tsukumo and Koji Yasutomo : The interplay between CD4 T cells and fibroblasts in salivary glands drives autoimmune pathology in Sjögrens syndrome, 11th International Conference on Autoimmunity: Mechanisms and NovelTreatments; Aegean Conference, Oct. 2024.
2.	Shogo Miyamura, Ryo Oe, Takuya Nakahara, Shota Okada, Shuji Taue, Yu Tokizane, Takeo Minamikawa, Taka-aki Yano, Kunihiro Otsuka, Ayuko Sakane, Takuya Sasaki, Koji Yasutomo, Taira Kajisa and Takeshi Yasui : Rapid detection of SARS- CoV-2 nucleocapsid protein antigen by dual- comb biosensing, SPIE Biomedical Imaging and Sensing Conference 2022 (BISC2022), 250308, Taipei, Dec. 2022.
3.	MIYAMURA Shogo, Ryo Oe, Takuya Nakahara, Shota Okada, Taira Kajisa, Shuji Taue, Yu Tokizane, Takeo Minamikawa, Taka-aki Yano, Kunihiro Otsuka, Ayuko Sakane, Takuya Sasaki, Koji Yasutomo and Takeshi Yasui : Dual-Comb Biosensing for Rapid Detection of SARS-CoV-2, Conference on Lasers and Electro-Optics 2022 (CLEO2022), JTh6A.6, San Jose, May 2022. (文献検索サイトへのリンク) ● Summary page in Scopus @ Elsevier: 2-s2.0-85139913953 (Elsevier: Scopus)
4.	HIRANKARN Nattiya, CLIMACOSA Monica Fresthel and Kunihiro Otsuka : Genetics, Immunological and Neurological Long-term Consequences in Prospective COVID-19 Cohort in Thailand, Japan, Philippines and USA, Science, Technology and Innovation (STI) for Global Challenges, Dec. 2021.

国内講演発表:

1.	Rinna Koga, Junko Morimoto, Kunihiro Otsuka and Koji Yasutomo : Proteasome dysfunction in adipocytes induces lipodystrophy and autoinflammation, 第53回日本免疫学会学術集会, Dec. 2024.
2.	Kunihiro Otsuka, Hiroyuki Kondo, Shin-ichi Tsukumo, Naozumi Ishimaru and Koji Yasutomo : Salivary gland fibroblasts drive autoimmune pathology via the interaction with CD4+ T cells in Sjögrens syndrome, 第53回日本免疫学会学術集会, Dec. 2024.
3.	西田真理, 大塚邦紘, 福場真美, 浪花耕平, 可児耕一, 桃田幸弘, 永尾瑠佳, 松澤鎮史, 牛尾綾, 常松貴明, 石丸直澄, 青田桂子 : シェーグレン症候群における老化関連B細胞の動態と発生機序の検討, 第32回日本シェーグレン症候群学会学術集会, 2024年9月.
4.	大塚邦紘, 近藤博之, 石丸直澄, 安友康二 : 線維芽細胞を介した自己免疫病変の増悪機構, 第32回日本シェーグレン症候群学会学術集会, 2024年9月.
5.	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におけるT Cell Receptor Associated Transmembrane Adaptor 1 (Trat1)を介した活性化T細胞抑制機構の解明, 第22回四国免疫フォーラム, 2024年6月.
6.	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.
7.	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.
8.	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.
9.	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.
10.	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.
11.	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.
12.	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.
13.	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.
14.	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.
15.	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.
16.	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.
17.	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.
18.	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.
19.	Rinna Koga, Junko Morimoto, Kunihiro Otsuka and Koji Yasutomo : Proteasome dysfunction in adipocytes induces lipodystrophy and autoinflammation, 第52回日本免疫学会学術集会, Jan. 2024.
20.	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.
21.	近藤博之, 岡部克生, 川阪安人, 大塚邦紘, 安友康二 : インフルエンザウイルス肺炎の免疫応答におけるマルチプレックス時空間解析とそこから発見した組織修復性CD4陽性T細胞の解析, 第46回日本分子生物学会年会, 2023年12月.
22.	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.
23.	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.
24.	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.
25.	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.
26.	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.
27.	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.
28.	大塚邦紘, 石丸直澄, 安友康二 : CD153+ CD4+ T cellによるシェーグレン症候群の新たな発症機序の解明, 第5回口腔医科学フロンティア研究会, 2023年4月.
29.	田村海, 川人祐樹, 佐藤真美, 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, 2023年4月.
30.	川人祐樹, 田村海, 佐藤真美, 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, 2023年4月.
31.	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.
32.	岡部克生, 大塚邦紘, 近藤博之, 安友康二 : インフルエンザウイルス肺炎の免疫応答に関するマルチプレックス時空間解析, 第112回日本病理学会総会, 2023年4月.
33.	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.
34.	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.
35.	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.
36.	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.
37.	宮村祥吾, 麻植凌, 仲原拓弥, 岡田昇太, 田上周路, 時実悠, 南川丈夫, 矢野隆章, 大塚邦紘, 坂根亜由子, 佐々木卓也, 安友康二, 加治佐平, 安井武史 : デュアル光コムバイオセンシングによるSARS-CoV-2/NP抗原の迅速·高感度検出, 学術講演会第43回年次大会, E06-19p-IX-01, 2023年1月.
38.	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.
39.	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.
40.	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.
41.	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.
42.	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.
43.	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.
44.	俵宏彰, 常松貴明, 永尾瑠佳, 佐藤真美, 大塚邦紘, 石丸直澄 : 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, 2022年12月.
45.	近藤博之, 九十九伸一, 大塚邦紘, 安友康二 : Markers of memory CD8 T cells depicting the effect of the BNT162b2 mRNA COVID-19 vaccine in Japan, 第45回日本分子生物学会年会, 2022年11月.
46.	大塚邦紘 : シェーグレン症候群の基礎研究について, 第33回日本臨床口腔病理学会, 2022年9月.
47.	大塚邦紘, 近藤博之, 九十九伸一, 新垣理恵子, 佐藤真美, 常松貴明, 石丸直澄, 安友康二 : 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, 2022年9月.
48.	宮村祥吾, 麻植凌, 仲原拓弥, 岡田昇太, 加治佐平, 時実悠, 南川丈夫, 矢野隆章, 田上周路, 大塚邦紘, 坂根亜由子, 佐々木卓也, 安友康二, 安井武史 : 新型コロナウイルスNタンパク抗原のデュアル光コム・バイオセンシング, 第83回応用物理学会秋季学術講演会, 21a-A200-4, 2022年9月.
49.	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.
50.	川人祐樹, 田村海, 佐藤真美, 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, 2022年9月.
51.	大塚邦紘, 九十九伸一, 近藤博之, 佐藤真美, 俵宏彰, 常松貴明, 石丸直澄, 安友康二 : 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, 2022年9月.
52.	田村海, 川人祐樹, 佐藤真美, 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, 2022年9月.
53.	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.
54.	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.
55.	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.
56.	近藤博之, 大塚邦紘, 九十九伸一, 安友康二 : 日本における新型SARS-CoV-2 mRNAワクチンBNT162b2の効果を示すメモリーCD8T細胞マーカー, 第20回四国免疫フォーラム, 2022年6月.
57.	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.
58.	常松貴明, 俵宏彰, 田中秀卓, 福田一稀, 佐藤真美, 大塚邦紘, 新垣理恵子, 石丸直澄 : 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, 2022年4月.
59.	大塚邦紘, 九十九伸一, 近藤博之, 新垣理恵子, 石丸直澄, 安友康二 : 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111回日本病理学会総会, 2022年4月.
60.	佐藤真美, 常松貴明, 大塚邦紘, 石丸直澄 : 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), 2022年2月.
61.	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.
62.	Yuki Sasaki, Hideki Arimochi, Kunihiro Otsuka, Hiroyuki Kondo, Shin-ichi Tsukumo and Koji Yasutomo : Blockade of the CXCR3-CXCL10 axis ameliorates inflammatory responses caused by immunoproteasome dysfunctions, 第50回日本免疫学会学術集会, Dec. 2021.
63.	俵宏彰, 新垣理恵子, 大塚邦紘, 石丸直澄 : シェーグレン症候群モデルマウスを用いたM3PAMを用いた治療効果とその作用機序, 第29回日本シェーグレン症候群学会学術集会, 2021年9月.
64.	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, 2021年9月.
65.	仲原拓弥, 麻植凌, 加治佐平, 時実悠, 南川丈夫, 田上周路, 大塚邦紘, 坂根亜由子, 安友康二, 佐々木卓也, 安井武史 : 屈折率センシング光コムを用いたバイオセンシングに関する検討(4)~新型コロナウイルス(SARS-CoV-2)の検出~, 第82回応用物理学会秋季学術講演会予稿集, 13p-N322-7, 2021年9月.
66.	大塚邦紘 : シェーグレン症候群モデルマウスを用いた病態解析, 第32回日本臨床口腔病理学会若手シンポジウム1 (炎症と再生), 2021年8月.
67.	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.
68.	Boonchan Michittra, Hideki Arimochi, Kunihiro Otsuka, Tomoko Kobayashi, Hisanori Uehara, Jaroonwitchawan Thiranut, Yuki Sasaki, Shin-ichi Tsukumo and Koji Yasutomo : Deficiency in Ripk3 or Mlkl exacerbates acute pancreatitis with increased apoptosis of acinar cell, 第19回四国免疫フォーラム, Jun. 2021.
69.	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.
70.	加治佐平, 矢野隆章, 大塚邦紘, 九十九伸一, 坂根亜由子, 駒貴明, 野間口雅子, 安友康二, 佐々木卓也, 安井武史 : SARS-CoV-2由来RNAの高感度検出に向けたプラズモニックバイオセンサ, 第68回応用物理学会春季学術講演会予稿集, 16p-Z22-13, 2021年3月.
71.	佐藤真美, 常松貴明, 大塚邦紘, 石丸直澄 : 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, 2021年2月.
72.	平尾功治, 湯本浩通, 大塚邦紘, 石丸直澄, 松尾敬志 : 歯内由来病変と混同しやすい根尖病変様のエックス線透過像を有する症例, 第18回西日本歯内療法学会会研修会(2018年度), 2018年9月.

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

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 )
CD153-CD30相互作用を介したシェーグレン症候群の新たな発症機序の解明 (研究課題/領域番号: 23K15976 )
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 )
シングルセルRNAシークエンス解析を基盤としたシェーグレン症候群の病態解明 (研究課題/領域番号: 20K18479 )
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 )
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助教 : 大塚邦紘