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Increased expression of TRAIL receptor 3 on eosinophils in churg-strauss syndrome
http://hdl.handle.net/2297/3654
http://hdl.handle.net/2297/3654dc23847b-302a-4334-960b-eb7c9b1b2040
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
HO-PR-WADA-T-662.pdf (575.8 kB)
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| Item type | 学術雑誌論文 / Journal Article(1) | |||||
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| 公開日 | 2017-10-05 | |||||
| タイトル | ||||||
| タイトル | Increased expression of TRAIL receptor 3 on eosinophils in churg-strauss syndrome | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| 資源タイプ | ||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
| 資源タイプ | journal article | |||||
| 著者 |
Mitsuyama, Hideo
× Mitsuyama, Hideo× Matsuyama, Wataru× Watanabe, Masaki× Shirahama, Yuko× Higashimoto, Ikkou× Wada, Takashi× Osame, Mitsuhiro× Arimura, Kimiyoshi |
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| 提供者所属 | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | 金沢大学医学部附属病院血液浄化療法部 | |||||
| 書誌情報 |
Arthritis and Rheumatism 巻 56, 号 2, p. 662-673, 発行日 2007-02-01 |
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| ISSN | ||||||
| 収録物識別子タイプ | ISSN | |||||
| 収録物識別子 | 0004-3591 | |||||
| DOI | ||||||
| 関連タイプ | isVersionOf | |||||
| 識別子タイプ | DOI | |||||
| 関連識別子 | https://doi.org/10.1002/art.22387 | |||||
| 出版者 | ||||||
| 出版者 | John Wiley & Sons | |||||
| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | Objective. Prolonged survival of eosinophils plays au important role in the pathogenesis of Churg-Strauss syndrome (CSS); however, its detailed molecular mechanism is still unclear. TRAIL and its receptors are expressed on a variety of cells, including eosinophils. In this study, we examined the expression of TRAIL receptors on eosinophils from patients with CSS. Methods. TRAIL receptor expression was assessed on eosinophils from healthy volunteers, patients with CSS, patients with asthma, and patients with hypereosinophilia due to parasitic infection. TRAIL-induced apoptosis of eosinophils was compared between the patients with CSS and patients with asthma. RNA interference was used to assess the effects of suppression of TRAIL receptor 3. Results. Expression of TRAIL receptor 3, a decoy receptor that acts as an antiapoptotic receptor, on eosinophils from patients with CSS was significantly higher than that in the other subjects. Moreover, in CSS, serum TRAIL receptor 3 levels showed a significant positive correlation with peripheral eosinophil counts, tissue-infiltrating eosinophils stained positive for this receptor, and peripheral T cells expressed TRAIL on their surface. Compared with asthma patients, eosinophils from CSS patients showed a significantly lower percentage of recombinant TRAIL, less autologous T cell-induced apoptosis, and decreased level of active caspase 3. Suppression of TRAIL receptor 3 through RNA interference significantly increased the recombinant TRAIL-induced apoptosis of eosinophils from CSS patients. Conclusion. Increased expression of TRAIL receptor 3 on eosinophils from patients with CSS was observed. These alterations in TRAIL receptor 3 expression might be involved in the molecular pathogenesis of CSS eosinophilia. © 2007, American College of Rheumatology. | |||||
| 著者版フラグ | ||||||
| 出版タイプ | AM | |||||
| 出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||
