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This review article discusses the innate immune system with a focus on Toll-like receptors (TLRs), bacterial endotoxin, and TLR4 signaling pathways, explaining their roles and activation mechanisms. It summarizes evidence that innate immune regulation can influence endometriosis progression in the pelvic environment, noting that growth can continue in ovariectomized animals and that increased macrophage infiltration has been reported in endometriosis tissue and peritoneal fluid. The paper also outlines how endotoxin involvement may contribute to adverse reproductive outcomes, but as a review it does not present new experimental data or specify a systematic limitations framework beyond its narrative synthesis. This paper is centrally about endometriosis — it reviews bacterial endotoxin and TLR4-related innate immune mechanisms in endometrium and endometriosis.
Abstract
Macrophages, dendritic cells, and Toll-like receptors (TLRs) are integral components of the innate immune system. This rapidly reactive system responds immediately to infectious or other non-self agents, thereby inducing an inflammatory response to protect the host until the activation of the slower adaptive immune system. The fundamentals of the innate immune system, functional characteristics of TLRs, and signaling pathways of TLR4 are discussed for the easy understanding by readers. Studies showed that the growth and progression of endometriosis continue even in ovariectomized animals. This indicates that besides ovarian steroid hormones, the growth of endometriosis can be regulated by the innate immune system in the pelvic environment. As a component of the innate immune system, increased infiltration of macrophages has been described in the intact tissue and peritoneal fluid of women with endometriosis. In this review article, we discuss the role of bacterial endotoxin and TLR4 in endometrium and endometriosis and outline the involvement of endotoxin in causing adverse reproductive outcome.
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アイテム
Toll-Like Receptors in Innate Immunity: Role of Bacterial Endotoxin and Toll-Like Receptor 4 in Endometrium and Endometriosis.
http://hdl.handle.net/10069/22001
http://hdl.handle.net/10069/22001bd38c56c-7eab-485f-90a5-3f4e439da6b9
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
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GOI68_40.pdf (559.4 kB)
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| アイテムタイプ | 学術雑誌論文 / Journal Article(1) | |||||||||||||||||||
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| 公開日 | 2009-06-19 | |||||||||||||||||||
| タイトル | ||||||||||||||||||||
| タイトル | Toll-Like Receptors in Innate Immunity: Role of Bacterial Endotoxin and Toll-Like Receptor 4 in Endometrium and Endometriosis. | |||||||||||||||||||
| 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 |
Khan, Khaleque Newaz
× Khan, Khaleque Newaz
× Kitajima, Michio
× Hiraki, Koichi
× Fujishita, Akira
× Sekine, Ichiro
× Ishimaru, Tadayuki
× Masuzaki, Hideaki
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| 抄録 | ||||||||||||||||||||
| 内容記述タイプ | Abstract | |||||||||||||||||||
| 内容記述 | Macrophages, dendritic cells, and Toll-like receptors (TLRs) are integral components of the innate immune system. This rapidly reactive system responds immediately to infectious or other non-self agents, thereby inducing an inflammatory response to protect the host until the activation of the slower adaptive immune system. The fundamentals of the innate immune system, functional characteristics of TLRs, and signaling pathways of TLR4 are discussed for the easy understanding by readers. Studies showed that the growth and progression of endometriosis continue even in ovariectomized animals. This indicates that besides ovarian steroid hormones, the growth of endometriosis can be regulated by the innate immune system in the pelvic environment. As a component of the innate immune system, increased infiltration of macrophages has been described in the intact tissue and peritoneal fluid of women with endometriosis. In this review article, we discuss the role of bacterial endotoxin and TLR4 in endometrium and endometriosis and outline the involvement of endotoxin in causing adverse reproductive outcome. | |||||||||||||||||||
| 書誌情報 |
Gynecologic and obstetric investigation 巻 68, 号 1, p. 40-52, 発行日 2009-04-09 |
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| 出版者 | ||||||||||||||||||||
| 出版者 | S. Karger AG | |||||||||||||||||||
| ISSN | ||||||||||||||||||||
| 収録物識別子タイプ | ISSN | |||||||||||||||||||
| 収録物識別子 | 03787346 | |||||||||||||||||||
| EISSN | ||||||||||||||||||||
| 収録物識別子タイプ | ISSN | |||||||||||||||||||
| 収録物識別子 | 1423-002X | |||||||||||||||||||
| PubMed番号 | ||||||||||||||||||||
| 関連タイプ | isVersionOf | |||||||||||||||||||
| 識別子タイプ | PMID | |||||||||||||||||||
| 関連識別子 | 19365133 | |||||||||||||||||||
| DOI | ||||||||||||||||||||
| 関連タイプ | isVersionOf | |||||||||||||||||||
| 識別子タイプ | DOI | |||||||||||||||||||
| 関連識別子 | 10.1159/000212061 | |||||||||||||||||||
| 権利 | ||||||||||||||||||||
| 権利情報 | Copyright (c) 2009 S. Karger AG, Basel | |||||||||||||||||||
| 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 | |||||||||||||||||||
| 引用 | ||||||||||||||||||||
| 内容記述タイプ | Other | |||||||||||||||||||
| 内容記述 | Gynecologic and Obstetric Investigation, 68(1), pp.40-52; 2009 |
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