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45 results on '"Hashimoto, Kahoko"'

2. Supplementary Figures 1-13 from Memory Type 2 Helper T Cells Induce Long-Lasting Antitumor Immunity by Activating Natural Killer Cells

Author

Kitajima, Masayuki, primary, Ito, Toshihiro, primary, Tumes, Damon J., primary, Endo, Yusuke, primary, Onodera, Atsushi, primary, Hashimoto, Kahoko, primary, Motohashi, Shinichiro, primary, Yamashita, Masakatsu, primary, Nishimura, Takashi, primary, Ziegler, Steven F., primary, and Nakayama, Toshinori, primary

Published
2023
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23. Enhanced Th2 Cell Differentiation and Allergen-Induced Airway Inflammation in Zfp35-Deficient Mice

Author

Kitajima, Masayuki, primary, Iwamura, Chiaki, additional, Miki-Hosokawa, Takako, additional, Shinoda, Kenta, additional, Endo, Yusuke, additional, Watanabe, Yukiko, additional, Shinnakasu, Ryo, additional, Hosokawa, Hiroyuki, additional, Hashimoto, Kahoko, additional, Motohashi, Shinichiro, additional, Koseki, Haruhiko, additional, Ohara, Osamu, additional, Yamashita, Masakatsu, additional, and Nakayama, Toshinori, additional

Published
2009
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29. Primary structure of the heparin-binding site of type V collagen

Author

Kazuhiko Takahara, Ikunoshin Kato, Manabu Ito, Hashimoto Kahoko, Yoshihito Yaoi, and Hiroyuki Koitabashi

Subjects
Stereochemistry, Molecular Sequence Data, Biophysics, Cleavage (embryo), Biochemistry, Peptide Mapping, Chromatography, Affinity, Affinity chromatography, medicine, Animals, Humans, Amino Acid Sequence, Binding site, Molecular Biology, Peptide sequence, Chromatography, High Pressure Liquid, chemistry.chemical_classification, Binding Sites, Chemistry, Heparin, Protein primary structure, Peptide Fragments, Enzyme, Ionic strength, Cattle, Collagen, medicine.drug, Peptide Hydrolases
Abstract

The abilities of collagens, type I, II, III, IV, and V, to bind heparin were examined by heparin-affinity chromatography and binding studies with [35S]heparin. At a physiological pH and ionic strength, only type V collagen bound to heparin. Collagens type I and II showed higher affinities than types III and IV for heparin, but did not bind to a heparin column at a physiological ionic strength. The heparin binding site of type V collagen was located in a 30 kDa CNBr fragment of the alpha 1(V) chain, and the amino acid sequence of this fragment was determined. The 30 kDa fragment contained a cluster of basic amino acid residues, and enzymatic cleavage within this basic domain greatly reduced the heparin-binding activities of the resulting peptides. Thus this basic region is probably the heparin-binding site of type V collagen.

Published
1990

41. Prolonged skin allograft survival by <it>IL-10</it> gene-introduced CD4 T cell administration

Author

Miyamoto, Takeshi, Kaneko, Takaaki, Yamashita, Masakatsu, Tenda, Yoshiyuki, Inami, Masamichi, Suzuki, Akane, Ishii, Sohtaro, Kimura, Motoko, Hashimoto, Kahoko, Shimada, Hideaki, Yahata, Hiroshi, Ochiai, Takenori, Saito, Izumu, DeGregori, James, and Nakayama, Toshinori

Abstract

Both CD4 and CD8 T cells play crucial roles in immune responses in transplantation. Immunosuppressive drugs, such as FK506 and cyclosporin A, block the priming of alloreactive CD4 Th cells and the subsequent induction of allospecific CD8 cytotoxic effector T cells and inhibit allograft rejection. However, the desire to minimize chronic complications that may arise from the use of immunosuppressive agents drives the search for additional strategies for immunosuppression of allograft rejection. In this study, CD4 or CD8 T cells into which the IL-10 gene is introduced using an adenovirus vector containing human IL-10 (hIL-10) cDNA (Ad-hIL-10) and into mouse T cells transgenic for the Coxsackie virus and adenovirus receptor form a model system to study the effect of administration of IL-10-secreting T cells on the survival of the allogenic skin grafts. Ad-hIL-10-infected CD4 and CD8 T cells secreted a large amount of hIL-10 for 3–4 days in culture in vitro. Ad-hIL-10-infected CD4 T cells administered in vivo could be detected in the spleen for 7 days post-transfer. Significantly prolonged survival of grafts was observed in animals that received either Ad-hIL-10-infected activated CD4 T cells or Th2-skewed CD4 T cells as compared with controls. Furthermore, substantial enhancement of the effect was observed in B6.C-H2bm1/ByJ transplants. Thus, a direct manipulation of T cells through the introduction of the immunosuppressive cytokine gene IL-10 may be a novel strategy for the control of allograft rejection.

Published
2005
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43. Memory type 2 helper T cells induce long-lasting antitumor immunity by activating natural killer cells

Author

Damon J. Tumes, Toshihiro Ito, Toshinori Nakayama, Kahoko Hashimoto, Takashi Nishimura, Steven F. Ziegler, Masakatsu Yamashita, Shinichiro Motohashi, Yusuke Endo, Masayuki Kitajima, Atsushi Onodera, Kitajima, Masayuki, Ito, Toshihiro, Tumes, Damon J, Endo, Yusuke, Onodera, Atsushi, Hashimoto, Kahoko, Motohashi, Shinichiro, Yamashita, Masakatsu, Nishimura, Takashi, Ziegler, Steven F, and Nakayama, Toshinori

Subjects
Cytotoxicity, Immunologic, Cancer Research, Mice, Nude, Mice, Transgenic, Cell Growth Processes, Lymphocyte Activation, Immunotherapy, Adoptive, Cell therapy, killer cells, Interleukin 21, Mice, Lymphocytes, Tumor-Infiltrating, Th2 Cells, Cytotoxic T cell, Animals, Interleukin 4, natural, Mice, Inbred BALB C, immunologic memory, biology, Chemistry, Histone-Lysine N-Methyltransferase, Neoplasms, Experimental, Natural killer T cell, Granzyme B, Killer Cells, Natural, Mice, Inbred C57BL, Th2 cells, Oncology, Perforin, biology.protein, Cancer research, Interleukin 12, Interleukin-4, Immunologic Memory, Myeloid-Lymphoid Leukemia Protein
Abstract

Functionally polarized helper T cells (Th cells) play crucial roles in the induction of tumor immunity. There is considerable knowledge about the contributions of IFN-producing Th1 cells that supports the role of cytotoxic cluster of differentiation (CD8) T cells and natural killer (NK) cells, but much less is known about how IL-4–producing Th2 cells contribute to tumor immunity. In this study, we investigated the cellular and molecular mechanisms employed by memory Th2 cells in sustaining tumor immunity by using a mouse model system wherein ovalbumin (OVA) is used as a specific tumor antigen. In this model, we found that OVA-specific memory Th2 cells exerted potent and long-lasting antitumor effects against NK-sensitive OVA-expressing tumor cells, wherein antitumor effects were mediated by NK cells. Specifically, NK cell cytotoxic activity and expression of perforin and granzyme B were dramatically enhanced by the activation of memory Th2 cells. Interleukin 4 (IL-4) produced by memory Th2 cells in vivo was critical for the antitumor effects of the NK cells, which IL-4 directly stimulated to induce their perforin- and granzyme-B–dependent cytotoxic activity. Our findings show that memory Th2 cells can induce potent antitumor immunity through IL-4–induced activation of NK cells, suggesting potential applications in cellular therapy for cancer patients. Cancer Res; 71(14); 4790–8. ©2011 AACR.

Published
2011

44. Synthesis of cinnamyl ethers from α-vinylbenzyl alcohol using iodine as catalyst.

Author

Kasashima Y, Uzawa A, Hashimoto K, Nishida T, Murakami K, Mino T, Sakamoto M, and Fujita T

Subjects
Carbamates chemistry, Catalysis, Ethers chemistry, Magnetic Resonance Spectroscopy standards, Molecular Structure, Reference Standards, Stereoisomerism, Carbamates chemical synthesis, Ethers chemical synthesis, Iodine chemistry, Propanols chemistry
Abstract

Reactions of α-vinylbenzyl alcohol with other alcohols using iodine as a catalyst were investigated. The corresponding cinnamyl ethers were obtained as products. This suggested that α-vinylbenzyl alcohol was converted to cinnamyl ethers via 1-phenylallyl cation. Cinnamyl ethyl ether was obtained in 75% yield by the reaction of α-vinylbenzyl alcohol and ethanol in acetonitrile with iodine under the following conditions: temperature = 50 °C, molar ratio of α-vinylbenzyl alcohol:ethanol:iodine = 1:3.0:0.2, and time period = 6 h. Generally, the yields of the reactions using primary alcohols were higher than those using secondary and tertiary alcohols. Ether interchange also occurred by the reaction of α-vinylbenzyl alcohol and iodine, but proceeded smoothly only when an allyl group was used as the other substituent of the starting ether.

Published
2010
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45. CD69 controls the pathogenesis of allergic airway inflammation.

Author

Miki-Hosokawa T, Hasegawa A, Iwamura C, Shinoda K, Tofukuji S, Watanabe Y, Hosokawa H, Motohashi S, Hashimoto K, Shirai M, Yamashita M, and Nakayama T

Subjects
Allergens administration & dosage, Allergens immunology, Animals, Antibodies, Monoclonal administration & dosage, Antibodies, Monoclonal therapeutic use, Antigens, CD genetics, Antigens, CD immunology, Antigens, Differentiation, T-Lymphocyte genetics, Antigens, Differentiation, T-Lymphocyte immunology, Asthma immunology, Asthma pathology, Bronchial Hyperreactivity immunology, Bronchial Hyperreactivity pathology, Bronchial Hyperreactivity prevention & control, Disease Models, Animal, Eosinophils immunology, Eosinophils pathology, Inflammation Mediators metabolism, Lectins, C-Type genetics, Lectins, C-Type immunology, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Knockout, Mice, Transgenic, Ovalbumin administration & dosage, Ovalbumin immunology, Respiratory Hypersensitivity prevention & control, Antigens, CD physiology, Antigens, Differentiation, T-Lymphocyte physiology, Inflammation Mediators physiology, Lectins, C-Type physiology, Respiratory Hypersensitivity immunology, Respiratory Hypersensitivity pathology
Abstract

Airway inflammation and airway hyperresponsiveness are central issues in the pathogenesis of asthma. CD69 is a membrane molecule transiently expressed on activated lymphocytes, and its selective expression in inflammatory infiltrates suggests that it plays a role in the pathogenesis of inflammatory diseases. In CD69-deficient mice, OVA-induced eosinophilic airway inflammation, mucus hyperproduction, and airway hyperresponsiveness were attenuated. Cell transfer of Ag-primed wild-type but not CD69-deficient CD4 T cells restored the induction of allergic inflammation in CD69-deficient mice, indicating a critical role of CD69 expressed on CD4 T cells. Th2 responses induced by CD69-deficient CD4 T cells in the lung were attenuated, and the migration of CD4 T cells into the asthmatic lung was severely compromised. The expression of VCAM-1 was also substantially altered, suggesting the involvement of VCAM-1 in the CD69-dependent migration of Th2 cells into the asthmatic lung. Interestingly, the administration of anti-CD69 Ab inhibited the induction of the OVA-induced airway inflammation and hyperresponsiveness. This inhibitory effect induced by the CD69 mAb was observed even after the airway challenge with OVA. These results indicate that CD69 plays a crucial role in the pathogenesis of allergen-induced eosinophilic airway inflammation and hyperresponsiveness and that CD69 could be a possible therapeutic target for asthmatic patients.

Published
2009
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