研究者詳細 - 前田　嘉信

MISC - 前田　嘉信

分割表示 319 件中 141 - 160 件目／全件表示 >>

alpha-Mannan induces Th17-mediated pulmonary graft-versus-host disease in mice 国際誌

Hidetaka Uryu, Daigo Hashimoto, Koji Kato, Eiko Hayase, Satomi Matsuoka, Reiki Ogasawara, Shuichiro Takahashi, Yoshinobu Maeda, Hiromi Iwasaki, Toshihiro Miyamoto, Shinobu Saijo, Yoichiro Iwakura, Geoffrey R. Hill, Koichi Akashi, Takanori Teshima

BLOOD 125 ( 19 ) 3014 - 3023 2015年5月

記述言語：英語出版者・発行元：AMER SOC HEMATOLOGY

Allogeneic hematopoietic stem cell transplantation (HSCT) is a curative therapy for various hematopoietic disorders. Graft-versus-host disease (GVHD) and infections are the major obstacles of HSCT, and their close relationship has been suggested. Although roles of bacterial and viral infections in the pathophysiology of GVHD are well described, impacts of fungal infection on GVHD remain to be elucidated. In mouse models of GVHD, injection of a-mannan (Mn), a major component of fungal cell wall, or heat-killed Candida albicans exacerbated GVHD, particularly in the lung. Mn-induced donor T-cell polarization toward Th17 and lung-specific chemokine environment in GVHD led to accumulation of Th17 cells in the lung. The detrimental effects of Mn on GVHD depended on donor IL-17A production and host C-type lectin receptor Dectin-2. These results suggest a previously unrecognized link between pulmonary GVHD and fungal infection after allogeneic HSCT.

DOI： 10.1182/blood-2014-12-615781

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自家末梢血造血幹細胞移植の前処置において、抗がん剤投与量はBMIに応じて増減すべきか

谷勝真, 藤原英晃, 西森久和, 松岡賢市, 藤井伸治, 近藤英生, 前田嘉信, 谷本光音, 廻勇輔, 小林優人, 藤井敬子

臨床血液 56 ( 5 ) 537 - 537 2015年5月

難治性Sweet病を合併したMDSに対して同種造血幹細胞移植を施行した1例

本倉恵美, 三道康永, 佐伯恭昌, 藤井伸治, 藤原英晃, 西森久和, 松岡賢市, 近藤英生, 前田嘉信, 谷本光音, 廻勇輔, 小林優人, 藤井敬子, 藤原暖, 土井裕子, 加持達弥, 岩月啓氏

臨床血液 56 ( 5 ) 538 - 538 2015年5月

同種造血幹細胞移植とGranulicatella adiacens敗血症

三道康永, 松岡賢市, 谷勝真, 能勢資子, 藤原英晃, 西森久和, 近藤英生, 藤井伸治, 前田嘉信, 谷本光音

臨床血液 56 ( 5 ) 538 - 538 2015年5月

当院において集中治療を要した造血幹細胞移植症例についての検討

中村真, 藤井伸治, 清家圭介, 三道康永, 石川立則, 藤原英晃, 西森和久, 松岡賢市, 近藤英生, 前田嘉信, 谷本光音

臨床血液 56 ( 5 ) 539 - 539 2015年5月

造血幹細胞移植後thrombotic microangiopathyに対するrecombinant thrombomodulin投与とその意義

藤原英晃, 前田嘉信, 三道康永, 中村真, 谷勝真, 石川隆則, 西森久和, 松岡賢市, 藤井伸治, 近藤英生, 谷本光音

臨床血液 56 ( 5 ) 534 - 534 2015年5月

Anti-IL-12/23 p40 Antibody Attenuates Experimental Chronic Graft-versus-Host Disease via Suppression of IFN-gamma/IL-17-Producing Cells 国際誌

Sachiyo Okamoto, Hideaki Fujiwara, Hisakazu Nishimori, Ken-ichi Matsuoka, Nobuharu Fujii, Eisei Kondo, Takehiro Tanaka, Akihiko Yoshimura, Mitsune Tanimoto, Yoshinobu Maeda

JOURNAL OF IMMUNOLOGY 194 ( 3 ) 1357 - 1363 2015年2月

記述言語：英語出版者・発行元：AMER ASSOC IMMUNOLOGISTS

Chronic graft-versus-host disease (GVHD) is a major cause of late death and morbidity after allogeneic hematopoietic cell transplantation. Recently, in addition to Th2 cells, Th1 and Th17 cells have been shown to contribute to chronic GVHD progression. IL-12 induces Th1 cells and IL-23 plays a role in stabilizing and/or amplifying Th17 cells, as well as in inducing IFN-gamma/IL-17 double-producing cells. Because mAb targeting the p40 subunit common to both IL-12 and IL-23 can inhibit both IL-12R and IL-23R-mediated signaling, we investigated the effects of anti-p40 mAb on a well-defined chronic GVHD mice model. Treatment of anti-p40 mAb in allogeneic recipients significantly reduced the severity of clinical and pathological chronic GVHD. Intracellular staining revealed that IFN-gamma single-positive (IL-17(-)) and IFN-gamma/IL-17 double-positive cells were suppressed in anti-p40 mAb-treated allogeneic recipients compared with control recipients. The cytokine levels of IFN-gamma and IL-17 were also decreased in serum from anti-p40 mAb-treated allogeneic recipients. T-bet expression of donor IL-17(+) CD4(+) T cells was reduced significantly in anti-p40 mAb-treated recipients, and this reduction in T-bet expression was associated with IL-22 production by donor T cells. These results suggested that anti-p40 mAb attenuated chronic GVHD via suppression of IFN-gamma/IL-17-producing cells, and that targeting the IL-12/IL-23 pathway may represent a promising therapeutic strategy for preventing and treating chronic GVHD.

DOI： 10.4049/jimmunol.1400973

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Impact of HLA Mismatch Direction on the Outcome of Unrelated Bone Marrow Transplantation: A Retrospective Analysis from the Japan Society for Hematopoietic Cell Transplantation 国際誌

Junya Kanda, Tatsuo Ichinohe, Shigeo Fuji, Yoshinobu Maeda, Kazuteru Ohashi, Takahiro Fukuda, Koichi Miyamura, Koji Iwato, Tetsuya Eto, Hirohisa Nakamae, Naoki Kobayashi, Takehiko Mori, Shin-ichiro Mori, Yasuo Morishima, Yoshiko Atsuta, Yoshinobu Kanda

BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION 21 ( 2 ) 305 - 311 2015年2月

記述言語：英語出版者・発行元：ELSEVIER SCIENCE INC

The relative desirability of an unrelated donor with a bidirectional 1-locus mismatch (1MM-Bi), a 1-locus mismatch only in the graft-versus-host direction (1MM-GVH), or a 1-locus mismatch only in the host-versus-graft direction (1MM-HVG) is not yet clear. We analyzed adult patients with leukemia or myelodys-plastic syndrome who received a first allogeneic stem cell transplant from an HLA-A, -B, -C, and -DRB1 matched or 1-allele mismatched unrelated donor in Japan. The effects of 1MM-Bi (n = 1020), 1MM-GVH (n = 83), and 1MM-HVG (n = 83) compared with a zero mismatch (0MM) (n = 2570) were analyzed after adjusting for other significant variables. The risk of grades III to IV acute graft-versus-host disease (GVHD) was higher with marginal significance in the 1MM-GVH group than in the 0MM group (hazard ratio, 1.85; P = .014). However, there was no significant difference in overall or nonrelapse mortality between the 1MM-GVH and 0MM groups. There was no significant difference in acute GVHD or overall or nonrelapse mortality between the 1MM-HVG and 0MM groups. The risks of acute GVHD and overall mortality were significantly higher in the 1MM-Bi group than in the 0MM group. These findings indicate that unrelated donors with 1MM-GVH and 1MM-HVG are both good candidates for patients without an HLA-matched unrelated donor in a Japanese cohort. (C) 2015 American Society for Blood and Marrow Transplantation.

DOI： 10.1016/j.bbmt.2014.10.015

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t(14;16)-positive multiple myeloma shows negativity for CD56 expression and unfavorable outcome even in the era of novel drugs

T. Narita, A. Inagaki, T. Kobayashi, Y. Kuroda, T. Fukushima, M. Nezu, S. Fuchida, H. Sakai, N. Sekiguchi, I. Sugiura, Y. Maeda, H. Takamatsu, N. Tsukamoto, D. Maruyama, Y. Kubota, M. Kojima, K. Sunami, T. Ono, M. Ri, K. Tobinai, S. Iida

BLOOD CANCER JOURNAL 5 2015年2月

Prospective Multicenter Phase II Study of HLA-Haploidentical Peripheral Blood Stem Cell Transplantation after Reduced-Intensity Conditioning with Post-Transplant Cyclophosphamide: First Analysis of the JSCT Haplo13 Study

Junichi Sugita, Naomi Kawashima, Tomoaki Fujisaki, Kazuhiko Kakihana, Naoyuki Uchida, Yoshinobu Maeda, Shuichi Ota, Keitaro Matsuo, Toshihiro Miyamoto, Koji Nagafuji, Tetsuya Eto, Koichi Akashi, Shuichi Taniguchi, Mine Harada, Takanori Teshima

BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION 21 ( 2 ) S313 - S314 2015年2月

Identification of transactivation-responsive DNA-binding protein 43 (TARDBP43; TDP-43) as a novel factor for TNF-α expression upon lipopolysaccharide stimulation in human monocytes.

Murata H, Hattori T, Maeda H, Takashiba S, Takigawa M, Kido J, Nagata T

Journal of Periodontal Research 50 ( 4 ) 452 - 460 2015年1月

© 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd. Background and Objective: Tumor necrosis factor alpha (TNF-α) is a major cytokine implicated in various inflammatory diseases. The nature of the nuclear factors associated with human TNF-α gene regulation is not well elucidated. We previously identified a novel region located from -550 to -487 in human TNF-α promoter that did not contain the reported binding sites for nuclear factor kappa B (NF-κB) but showed lipopolysaccharide (LPS)-induced transcriptional activity. The purpose of this study is to identify novel factors that bind to the promoter region and regulate TNF-α expression. Material and Methods: To identify DNA-binding proteins that bound to the target region of TNF-α promoter, a cDNA library from LPS-stimulated human monocytic cell line THP-1 was screened using a yeast one-hybrid system. Cellular localizations of the DNA-binding protein in the cells were examined by subcellular immunocytochemistry. Nuclear amounts of the protein in LPS-stimulated THP-1 cells were identified by western blot analysis. Expression of mRNA of the protein in the cells was quantified by real-time polymerase chain reaction. Electrophoretic mobility shift assays were performed to confirm the DNA-binding profile. Overexpression of the protein and knockdown of the gene were also performed to investigate the role for TNF-α expression. Results: Several candidates were identified from the cDNA library and transactivation-responsive DNA-binding protein 43 (TARDBP43; TDP-43) was focused on. Western blot analysis revealed that nuclear TDP-43 protein was increased in the LPS-stimulated THP-1 cells. Expression of TDP-43 mRNA was already enhanced before TNF-α induction by LPS. Electrophoretic mobility shift assay analysis showed that nuclear extracts obtained by overexpressing FLAG-tagged TDP-43 bound to the -550 to -487 TNF-α promoter fragments. Overexpression of TDP-43 in THP-1 cells resulted in an increase of TNF-α expression. Knockdown of TDP-43 in THP-1 cells downregulated TNF-α expression. Conclusion: We identified TDP-43 as one of the novel TNF-α factors and found that it bound to the LPS-responsive element in the TNF-α promoter to increase TNF-α expression.

DOI： 10.1111/jre.12227

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再発・難治性ホジキンリンパ腫に対するPD-1免疫チェックポイント阻害薬ニボルマブの有効性

前田嘉信

血液内科 71 ( 4 ) 487 - 492 2015年