書誌事項
- タイトル別名
-
- Death-inducing TNF family member-mediated cytotoxicity
- 公開日
- 2003
- DOI
-
- 10.2492/jsir.23.144
- 公開者
- 一般社団法人 日本炎症・再生医学会
この論文をさがす
説明
Killer cells such as CTL, NK cells, and monocytes play important roles in immune surveillance against transformed cells and virus-infected cells. CTL and NK cells directly kill target cells via two major effector pathways, the perforin-mediated and FasL-mediated pathways. In addition to these pathways, however, some studies by using the gene-targeting mice suggested the possible existence of some other effector mechanisms for the cytotoxicity. Monocytes not only mediate inflammatory responses via production of various cytokines and chemical mediators, but also kill directly some transformed cells. However the effector mechanisms remain largely unknown. Recently, some death-inducing TNF family members, such as TNF-related apoptosis-inducing ligand (TRAIL) and TWEAK were identified and it has been reported that TRAIL- and TWEAK-dependent mechanisms constitute novel pathways of killer cell cytotoxicity. FasL and TRAIL have also been implicated in the tissue damage associated with some inflammatory diseases, such as hepatitis and rheumatoid arthritis. This review describes the expression of FasL, TRAIL, and TWEAK on killer cells and discusses the pathophysiological roles of these molecules in immune system.
収録刊行物
-
- 炎症・再生
-
炎症・再生 23 (3), 144-150, 2003
一般社団法人 日本炎症・再生医学会
- Tweet
キーワード
詳細情報 詳細情報について
-
- CRID
- 1390282680155505152
-
- NII論文ID
- 130000165305
-
- NII書誌ID
- AA11508953
-
- ISSN
- 18805795
- 13468022
-
- 本文言語コード
- ja
-
- データソース種別
-
- JaLC
- Crossref
- CiNii Articles
- OpenAIRE
-
- 抄録ライセンスフラグ
- 使用不可