Teruko Tomono
Kyoto University
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Featured researches published by Teruko Tomono.
Gut | 2016
Masahiro Shiokawa; Yuzo Kodama; Katsutoshi Kuriyama; Kenichi Yoshimura; Teruko Tomono; Toshihiro Morita; Nobuyuki Kakiuchi; Tomoaki Matsumori; Atsushi Mima; Yoshihiro Nishikawa; Tatsuki Ueda; Motoyuki Tsuda; Yuki Yamauchi; Ryuki Minami; Yojiro Sakuma; Yuji Ota; Takahisa Maruno; Akira Kurita; Yugo Sawai; Yoshihisa Tsuji; Norimitsu Uza; Kazuyoshi Matsumura; Tomohiro Watanabe; Kenji Notohara; Tatsuaki Tsuruyama; Hiroshi Seno; Tsutomu Chiba
Objective IgG4-related disease (IgG4-RD) is a systemic disease characterised by elevated serum IgG4 and IgG4-positive lymphoplasmacytic infiltration in the affected tissues. The pathogenic role of IgGs, including IgG4, in patients with IgG4-RD, however, is unknown. Design We examined the pathogenic activity of circulating IgGs in patients with IgG4-RD by injecting their IgGs into neonatal male Balb/c mice. Binding of patient IgGs to pancreatic tissue was also analysed in an ex vivo mouse organ culture model and in tissue samples from patients with autoimmune pancreatitis (AIP). Results Subcutaneous injection of patient IgG, but not control IgG, resulted in pancreatic and salivary gland injuries. Pancreatic injury was also induced by injecting patient IgG1 or IgG4, with more destructive changes induced by IgG1 than by IgG4. The potent pathogenic activity of patient IgG1 was significantly inhibited by simultaneous injection of patient IgG4. Binding of patient IgG, especially IgG1 and IgG4, to pancreatic tissue was confirmed in both the mouse model and AIP tissue samples. Conclusions IgG1 and IgG4 from patients with IgG4-RD have pathogenic activities through binding affected tissues in neonatal mice.
PLOS ONE | 2017
Yu Uneno; Kei Taneishi; Masashi Kanai; Kazuya Okamoto; Yosuke Yamamoto; Akira Yoshioka; Shuji Hiramoto; Akira Nozaki; Yoshitaka Nishikawa; Daisuke Yamaguchi; Teruko Tomono; Masahiko Nakatsui; Mika Baba; Tatsuya Morita; Shigemi Matsumoto; Tomohiro Kuroda; Yasushi Okuno; Manabu Muto
Background We aimed to develop an adaptable prognosis prediction model that could be applied at any time point during the treatment course for patients with cancer receiving chemotherapy, by applying time-series real-world big data. Methods Between April 2004 and September 2014, 4,997 patients with cancer who had received systemic chemotherapy were registered in a prospective cohort database at the Kyoto University Hospital. Of these, 2,693 patients with a death record were eligible for inclusion and divided into training (n = 1,341) and test (n = 1,352) cohorts. In total, 3,471,521 laboratory data at 115,738 time points, representing 40 laboratory items [e.g., white blood cell counts and albumin (Alb) levels] that were monitored for 1 year before the death event were applied for constructing prognosis prediction models. All possible prediction models comprising three different items from 40 laboratory items (40C3 = 9,880) were generated in the training cohort, and the model selection was performed in the test cohort. The fitness of the selected models was externally validated in the validation cohort from three independent settings. Results A prognosis prediction model utilizing Alb, lactate dehydrogenase, and neutrophils was selected based on a strong ability to predict death events within 1–6 months and a set of six prediction models corresponding to 1,2, 3, 4, 5, and 6 months was developed. The area under the curve (AUC) ranged from 0.852 for the 1 month model to 0.713 for the 6 month model. External validation supported the performance of these models. Conclusion By applying time-series real-world big data, we successfully developed a set of six adaptable prognosis prediction models for patients with cancer receiving chemotherapy.
Scientific Reports | 2018
Yojiro Sakuma; Yuzo Kodama; Takaaki Eguchi; Norimitsu Uza; Yoshihisa Tsuji; Masahiro Shiokawa; Takahisa Maruno; Katsutoshi Kuriyama; Yoshihiro Nishikawa; Yuki Yamauchi; Motoyuki Tsuda; Tatsuki Ueda; Tomoaki Matsumori; Toshihiro Morita; Teruko Tomono; Nobuyuki Kakiuchi; Atsushi Mima; Yuko Sogabe; Saiko Marui; Takeshi Kuwada; Akihiko Okada; Tomohiro Watanabe; Hiroshi Nakase; Tsutomu Chiba; Hiroshi Seno
Severe acute pancreatitis is a lethal inflammatory disease frequently accompanied by pancreatic necrosis. We aimed to identify a key regulator in the development of pancreatic necrosis. A cytokine/chemokine array using sera from patients with acute pancreatitis (AP) revealed that serum CXCL16 levels were elevated according to the severity of pancreatitis. In a mouse model of AP, Cxcl16 expression was induced in pancreatic acini in the late phase with the development of pancreatic necrosis. Cxcl16−/− mice revealed similar sensitivity as wild-type (WT) mice to the onset of pancreatitis, but better resisted development of acinar cell necrosis with attenuated neutrophil infiltration. A cytokine array and immunohistochemistry revealed lower expression of Ccl9, a neutrophil chemoattractant, in the pancreatic acini of Cxcl16−/− mice than WT mice. Ccl9 mRNA expression was induced by stimulation with Cxcl16 protein in pancreatic acinar cells in vitro, suggesting a Cxcl16/Ccl9 cascade. Neutralizing antibody against Cxcl16 ameliorated pancreatic injury in the mouse AP model with decreased Ccl9 expression and less neutrophil accumulation. In conclusion, Cxcl16 expressed in pancreatic acini contributes to the development of acinar cell necrosis through the induction of Ccl9 and subsequent neutrophil infiltration. CXCL16 could be a new therapeutic target in AP.
Science Translational Medicine | 2018
Masahiro Shiokawa; Yuzo Kodama; Kiyotoshi Sekiguchi; Takeshi Kuwada; Teruko Tomono; Katsutoshi Kuriyama; Hajime Yamazaki; Toshihiro Morita; Saiko Marui; Yuko Sogabe; Nobuyuki Kakiuchi; Tomoaki Matsumori; Atsushi Mima; Yoshihiro Nishikawa; Tatsuki Ueda; Motoyuki Tsuda; Yuki Yamauchi; Yojiro Sakuma; Takahisa Maruno; Norimitsu Uza; Tatsuaki Tsuruyama; Tsuneyo Mimori; Hiroshi Seno; Tsutomu Chiba
The extracellular matrix protein laminin 511 is an autoantigen involved in the pathophysiology of autoimmune pancreatitis. Pancreatic perturbation Autoimmune pancreatitis (AIP) is difficult to diagnose and can sometimes be confused with pancreatic cancer, which presents with similar symptoms. AIP is an inflammatory disease involving elevated IgG4, but the target autoantigen(s) is unidentified. This group’s previous work pointed to the extracellular matrix, and now, Shiokawa et al. show that a truncated form of laminin 511 may be a major autoantigen in AIP. They observed that half of AIP patients they analyzed had anti–laminin 511 antibodies, which were absent in healthy controls. Patient pancreatic tissues were positive for laminin 511, and immunization of mice with this protein induced AIP-like symptoms. These results reveal an autoimmune target in this disease and one day may aid AIP diagnosis. Autoimmune pancreatitis (AIP), a major manifestation of immunoglobulin G4–related disease (IgG4-RD), is an immune-mediated disorder, but the target autoantigens are still unknown. We previously reported that IgG in patients with AIP induces pancreatic injuries in mice by binding the extracellular matrix (ECM). In the current study, we identified an autoantibody against laminin 511-E8, a truncated laminin 511, one of the ECM proteins, in patients with AIP. Anti–laminin 511-E8 IgG was present in 26 of 51 AIP patients (51.0%), but only in 2 of 122 controls (1.6%), by enzyme-linked immunosorbent assay. Because truncated forms of other laminin family members in other organs have been reported, we confirmed that truncated forms of laminin 511 also exist in human and mouse pancreas. Histologic studies with patient pancreatic tissues showed colocalization of patient IgG and laminin 511. Immunization of mice with human laminin 511-E8 induced antibodies and pancreatic injury, fulfilling the pathologic criteria for human AIP. Four of 25 AIP patients without laminin 511-E8 antibodies had antibodies against integrin α6β1, a laminin 511 ligand. AIP patients with laminin 511-E8 antibodies exhibited distinctive clinical features, as the frequencies of malignancies or allergic diseases were significantly lower in patients with laminin 511-E8 antibodies than in those without. The discovery of these autoantibodies should aid in the understanding of AIP pathophysiology and possibly improve the diagnosis of AIP.
International Journal of Clinical Oncology | 2017
Yoshitaka Nishikawa; Masashi Kanai; Maiko Narahara; Akiko Tamon; J.B. Brown; Kei Taneishi; Masahiko Nakatsui; Kazuya Okamoto; Yu Uneno; Daisuke Yamaguchi; Teruko Tomono; Yukiko Mori; Shigemi Matsumoto; Yasushi Okuno; Manabu Muto
Gastroenterology | 2018
Toshihiro Morita; Yuzo Kodama; Hiroshi Seno; Norimitsu Uza; Masahiro Shiokawa; Takahisa Maruno; Motoyuki Tsuda; Tatsuki Ueda; Yoshihiro Nishikawa; Yuki Yamauchi; Tomoaki Matsumori; Nobuyuki Kakiuchi; Teruko Tomono; Atsushi Mima; Takeshi Kuwada; Saiko Marui; Yuko Sogabe; Hirokazu Okada; Tomonori Hirano; Yojiro Sakuma; Katsutoshi Kuriyama
Gastroenterology | 2018
Yoshihiro Nishikawa; Yuzo Kodama; Hirokazu Okada; Takeshi Kuwada; Saiko Marui; Teruko Tomono; Tomoaki Matsumori; Toshihiro Morita; Yuki Yamauchi; Masahiro Shiokawa; Norimitsu Uza; Hiroshi Seno
Gastroenterology | 2018
Tomoaki Matsumori; Yuzo Kodama; Norimitsu Uza; Masahiro Shiokawa; Yoshihiro Nishikawa; Yuki Yamauchi; Toshihiro Morita; Teruko Tomono; Takeshi Kuwada; Saiko Marui; Hirokazu Okada; Hiroshi Seno
Gastroenterology | 2017
Yuki Yamauchi; Yuzo Kodama; Yuko Sogabe; Takeshi Kuwada; Saiko Marui; Atsushi Mima; Teruko Tomono; Toshihiro Morita; Nobuyuki Kakiuchi; Tomoaki Matsumori; Yoshihiro Nishikawa; Tatsuki Ueda; Motoyuki Tsuda; Katsutoshi Kuriyama; Yojiro Sakuma; Takahisa Maruno; Masahiro Shiokawa; Norimitsu Uza; Hiroshi Seno
Gastroenterology | 2016
Yojiro Sakuma; Yuzo Kodama; Tomoaki Matsumori; Teruko Tomono; Nobuyuki Kakiuchi; Atsushi Mima; Yuki Yamauchi; Yoshihiro Nishikawa; Motoyuki Tsuda; Tatsuki Ueda; Katsutoshi Kuriyama; Takahisa Maruno; Yuji Ota; Masahiro Shiokawa; Yoshihisa Tsuji; Norimitsu Uza; Tomohiro Watanabe; Hiroshi Nakase; Hiroshi Seno; Tsutomu Chiba