担持金属触媒における光熱変換型メタンドライリフォーミング反応に関する研究

京都大学新制・課程博士博士(人間・環境学)甲第24711号人博第1084号新制||人||254(附属図書館)2022||人博||1084(吉田南総合図書館)京都大学大学院人間・環境学研究科相関環境学専攻(主査)教授 吉田 寿雄, 教授 田部 勢津久, 教授 中村 敏浩, 教授 田中 庸裕学位規則第4条第1項該当Doctor of Human and Environmental StudiesKyoto UniversityDFA

Temperature-Graduated Nickel-Silica Catalysts for Photothermal Steam Reforming of Methane

Photothermal steam reforming of methane (PTSRM) is a promising catalytic technology for converting stable methane and water into hydrogen utilizing solar energy. In the present study, the photothermal catalytic activity of silica-supported nickel (Ni/SiO₂) catalysts was investigated using a gas-flow reactor under concentrated visible/near-infrared light irradiation with various experimental parameters to obtain insight into factors affecting the activity and selectivity. In the thermal SRM at 773 K in the dark, the CH₄ conversion reached near-equilibrium with all four Ni/SiO₂ catalysts, while there was a significant difference in activity between the catalysts in the PTSRM reaction under light irradiation. These results indicate that PTSRM activity was affected by both thermodynamic and kinetic aspects. The conversion–selectivity relationship revealed that the product selectivity in PTSRM was different from the values in thermal SRM in the dark and calculated thermodynamic equilibrium. We proposed that concentrated light irradiation created the highest temperature zone in the centre of the reactor and the lower temperature zone downstream, and the consecutive water gas shift reaction and CO hydrogenation occurred in the lower temperature zone, thus resulting in the characteristic product selectivity. This study shows the potential of PTSRM systems with controllable selectivity by the temperature gradients formed under concentrated sunlight irradiation

A circulating subset of iNKT cells mediates antitumor and antiviral immunity

新規の循環型iNKT細胞を発見 --抗腫瘍・抗ウイルス感染効果の高い免疫細胞療法の開発への貢献に期待--. 京都大学プレスリリース. 2022-10-24.Invariant natural killer T (iNKT) cells are a group of innate-like T lymphocytes that recognize lipid antigens. They are supposed to be tissue resident and important for systemic and local immune regulation. To investigate the heterogeneity of iNKT cells, we recharacterized iNKT cells in the thymus and peripheral tissues. iNKT cells in the thymus were divided into three subpopulations by the expression of the natural killer cell receptor CD244 and the chemokine receptor CXCR6 and designated as C0 (CD244⁻CXCR6⁻), C1 (CD244⁻CXCR6⁺), or C2 (CD244⁺CXCR6⁺) iNKT cells. The development and maturation of C2 iNKT cells from C0 iNKT cells strictly depended on IL-15 produced by thymic epithelial cells. C2 iNKT cells expressed high levels of IFN-γ and granzymes and exhibited more NK cell–like features, whereas C1 iNKT cells showed more T cell–like characteristics. C2 iNKT cells were influenced by the microbiome and aging and suppressed the expression of the autoimmune regulator AIRE in the thymus. In peripheral tissues, C2 iNKT cells were circulating that were distinct from conventional tissue-resident C1 iNKT cells. Functionally, C2 iNKT cells protected mice from the tumor metastasis of melanoma cells by enhancing antitumor immunity and promoted antiviral immune responses against influenza virus infection. Furthermore, we identified human CD244⁺CXCR6⁺ iNKT cells with high cytotoxic properties as a counterpart of mouse C2 iNKT cells. Thus, this study reveals a circulating subset of iNKT cells with NK cell–like properties distinct from conventional tissue-resident iNKT cells

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.

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