6 research outputs found

    銅触媒による有機ボロン酸エステルを用いた不斉付加反応及び不斉置換反応

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    京都大学0048新制・課程博士博士(理学)甲第16254号理博第3675号新制||理||1534(附属図書館)28863京都大学大学院理学研究科化学専攻(主査)教授 林 民生, 教授 丸岡 啓二, 教授 大須賀 篤弘学位規則第4条第1項該当Doctor of ScienceKyoto UniversityDA

    Synthesis of Quaternary Carbon Stereocenters by Copper-Catalyzed Asymmetric Allylic Substitution of Allyl Phosphates with Arylboronates

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    A copper-catalyzed asymmetric allylic substitution of γ,γ-disubstituted allyl phosphates with arylboronates has been developed for the construction of quaternary stereocenters. High regio- and enantioselectivities have been achieved by employing a hydroxy-bearing chiral <i>N</i>-heterocyclic carbene ligand, and both <i>E</i> and <i>Z</i> substrates provide the same enantiomer as the major product. The mechanistic aspect of this catalysis has also been investigated to find that a 1:1 copper/ligand complex is most likely responsible for the present asymmetric catalysis, and the reaction proceeds with almost perfect 1,3-<i>anti</i> stereochemistry with respect to the allylic electrophile

    Synthesis of Quaternary Carbon Stereocenters by Copper-Catalyzed Asymmetric Allylic Substitution of Allyl Phosphates with Arylboronates

    No full text
    A copper-catalyzed asymmetric allylic substitution of γ,γ-disubstituted allyl phosphates with arylboronates has been developed for the construction of quaternary stereocenters. High regio- and enantioselectivities have been achieved by employing a hydroxy-bearing chiral <i>N</i>-heterocyclic carbene ligand, and both <i>E</i> and <i>Z</i> substrates provide the same enantiomer as the major product. The mechanistic aspect of this catalysis has also been investigated to find that a 1:1 copper/ligand complex is most likely responsible for the present asymmetric catalysis, and the reaction proceeds with almost perfect 1,3-<i>anti</i> stereochemistry with respect to the allylic electrophile

    Lung group 2 innate lymphoid cells differentially depend on local IL-7 for their distribution, activation, and maintenance in innate and adaptive immunity-mediated airway inflammation.

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    Interleukin-7 (IL-7) is a cytokine critical for the development and maintenance of group 2 innate lymphoid cells (ILC2s). ILC2s are resident in peripheral tissues such as the intestine and lung. However, whether IL-7 produced in the lung plays a role in the maintenance and function of lung ILC2s during airway inflammation remains unknown. IL-7 was expressed in bronchoalveolar epithelial cells and lymphatic endothelial cells (LECs). To investigate the role of local IL-7 in lung ILC2s, we generated two types of IL-7 conditional knockout (IL-7cKO) mice: Sftpc-Cre (SPC-Cre) IL-7cKO mice specific for bronchial epithelial cells and type 2 alveolar epithelial cells and Lyve1-Cre IL-7cKO mice specific for LECs. In steady state, ILC2s were located near airway epithelia, although lung ILC2s were unchanged in the two lines of IL-7cKO mice. In papain-induced airway inflammation dependent on innate immunity, lung ILC2s localized near bronchia via CCR4 expression, and eosinophil infiltration and type 2 cytokine production were reduced in SPC-Cre IL-7cKO mice. In contrast, in house dust mite (HDM)-induced airway inflammation dependent on adaptive immunity, lung ILC2s localized near lymphatic vessels via their CCR2 expression 2 weeks after the last challenge. Furthermore, lung ILC2s were decreased in Lyve1-Cre IL-7cKO mice in the HDM-induced inflammation because of decreased cell survival and proliferation. Finally, administration of anti-IL-7 antibody attenuated papain-induced inflammation by suppressing the activation of ILC2s. Thus, this study demonstrates that IL-7 produced by bronchoalveolar epithelial cells and LECs differentially controls the activation and maintenance of lung ILC2s, where they are localized in airway inflammation

    Lung group 2 innate lymphoid cells differentially depend on local IL-7 for their distribution, activation, and maintenance in innate and adaptive immunity-mediated airway inflammation.

    No full text
    Interleukin-7 (IL-7) is a cytokine critical for the development and maintenance of group 2 innate lymphoid cells (ILC2s). ILC2s are resident in peripheral tissues such as the intestine and lung. However, whether IL-7 produced in the lung plays a role in the maintenance and function of lung ILC2s during airway inflammation remains unknown. IL-7 was expressed in bronchoalveolar epithelial cells and lymphatic endothelial cells (LECs). To investigate the role of local IL-7 in lung ILC2s, we generated two types of IL-7 conditional knockout (IL-7cKO) mice: Sftpc-Cre (SPC-Cre) IL-7cKO mice specific for bronchial epithelial cells and type 2 alveolar epithelial cells and Lyve1-Cre IL-7cKO mice specific for LECs. In steady state, ILC2s were located near airway epithelia, although lung ILC2s were unchanged in the two lines of IL-7cKO mice. In papain-induced airway inflammation dependent on innate immunity, lung ILC2s localized near bronchia via CCR4 expression, and eosinophil infiltration and type 2 cytokine production were reduced in SPC-Cre IL-7cKO mice. In contrast, in house dust mite (HDM)-induced airway inflammation dependent on adaptive immunity, lung ILC2s localized near lymphatic vessels via their CCR2 expression 2 weeks after the last challenge. Furthermore, lung ILC2s were decreased in Lyve1-Cre IL-7cKO mice in the HDM-induced inflammation because of decreased cell survival and proliferation. Finally, administration of anti-IL-7 antibody attenuated papain-induced inflammation by suppressing the activation of ILC2s. Thus, this study demonstrates that IL-7 produced by bronchoalveolar epithelial cells and LECs differentially controls the activation and maintenance of lung ILC2s, where they are localized in airway inflammation
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