Targeted reduction of CCR4+ cells is sufficient to suppress allergic airway inflammation 4

• Material Type: 博士論文
• ISSN: 2212-5345
• Title: Targeted reduction of CCR4+ cells is sufficient to suppress allergic airway inflammation
• Volume: 51 4
• Author/Editor: Honjo, Akifumi; Ogawa, Hirohisa; Azuma, Masahiko; Tezuka, Toshifumi; Sone, Saburo; Biragyn, Arya; Nishioka, Yasuhiko
• Author Heading: Honjo, Akifumi; Ogawa, Hirohisa; Azuma, Masahiko; Tezuka, Toshifumi; Sone, Saburo; Biragyn, Arya; Nishioka, Yasuhiko
• Publication, Distribution, etc.: The Japanese Respiratory Society|Elsevier
• Publication Date: 2013-06-22
• Publication Date (W3CDTF): 2013-06-22
• Alternative Title: CCR4陽性細胞の選択的減少は、アレルギー性気道炎症を抑制する
• Periodical title: Respiratory Investigation
• Degree grantor/type: 徳島大学
• Date Granted: 2013-11-28
• Date Granted (W3CDTF): 2013-11-28
• Dissertation Number: 甲第2653号
• Degree Type: 博士（医学）
• Conferring No. (Dissertation): 甲第2653号
• Text Language Code: eng
• Subject Heading: CCR4; TARC-PE38; allergic inflammation; airway hyperresponsiveness; bronchial asthma
• Target Audience: 一般
• Note (General): Back ground: Bronchial asthma is characterized by allergic airway inflammation involving C-C chemokine receptor type 4 (CCR4)-positive Th2 cells. As such, we hypothesize that the disease can be alleviated by targeted-elimination of CCR4+ cells. Thymus and activation-regulated chemokine (TARC)-PE38, a TARC fused the exotoxin fragment PE38 from Pseudomonas aeruginosa, has been shown to efficiently kill CCR4+ cells by delivering the exotoxin fragment PE38into CCR4+ cells. To test our hypothesis, we examined whether TARC-PE38could suppress allergic airway inflammation in a mouse model of house dust mite (HDM)-induced allergic airway inflammation.Methods: We evaluated the effect of TARC-PE38 on the major characteristics of HDM-induced allergic airway inflammation. Airway hyper responsiveness, lung histopathology, lung Th1/Th2 cell populations, and concentrations of Th1/Th2 cytokines in the lungs were assessed in HDM-sensitized and challenged mice in the presence and absence of TARC-PE38.Results: TARC-PE38 efficiently suppressed allergic airway inflammation by significantly reducing airway hyperresponsiveness, the overall area of inflammation, and goblet cell hyperplasia. In HDM-sensitized and challenged mice, TARC-PE38 specifically reduced the numbers of CCR4+ cells. This reduction was associated with a significant decrease in the production of Th2 cytokines in the airway, and a decrease in the number of leukocytes, including macrophages, eosinophils and lymphocytes, within the subepithelial area of the lungs and airway lumen.TARC-PE38 had no effect on Th1 cells.Conclusion: Our data suggest that the elimination of CCR4+ cells viaTARC-PE38 treatment is sufficient to control allergic airway inflammation and airway hyperresponsiveness.
• DOI: info:doi/10.1016/j.resinv.2013.04.007; https://doi.org/info:doi/10.1016/j.resinv.2013.04.007
• Persistent ID (NDL): info:ndljp/pid/9984204; https://dl.ndl.go.jp/pid/9984204
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• Acquisition Basis: 博士論文（自動収集）
• Date Accepted (W3CDTF): 2016-06-03T01:05:16+09:00
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• Periodical Title (URI): http://repo.lib.tokushima-u.ac.jp/105964
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