IL-2/IL-18 prevent the down-modulation of NKG2D by TGF-beta in NK cells via the c-Jun N-terminal kinase (JNK) pathway
- Authors
- Song, Hyunkeun; Hur, Dae Young; Kim, Kyung-Eun; Park, Hyunjeong; Kim, Taesung; Kim, Chul-woo; Bang, Saic; Cho, Dae-Ho
- Issue Date
- Jul-2006
- Publisher
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- Keywords
- NK cells; NKG2D; TGF-beta; IL-2; IL-18
- Citation
- CELLULAR IMMUNOLOGY, v.242, no.1, pp 39 - 45
- Pages
- 7
- Journal Title
- CELLULAR IMMUNOLOGY
- Volume
- 242
- Number
- 1
- Start Page
- 39
- End Page
- 45
- URI
- https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/15110
- DOI
- 10.1016/j.cellimm.2006.09.002
- ISSN
- 0008-8749
1090-2163
- Abstract
- TGF-beta is known to play a major role for the reduced NKG2D expression seen in cancer patients. However, the mechanisms for reduced TGF-beta-induced down-regulation of NKG2D are unclear. In this study, we observed that IL-2/IL-18 increased the NKG2D expression in the TGF-beta treated NK cell line in a dose-dependent manner. Incubation with the JNK inhibitor SP600125 inhibited the NKG2D expression induced by IL-2/IL-18 in the TGF-beta treated human NK cell line. Moreover, the NK cytotoxicity assay showed that the reduced NK cytotoxicity by TGF-beta was recovered by IL-2/IL-18 treatment. The results indicate that IL-2/IL-18 strongly prevented the TGF-beta-induced NKG2D down-regulation in NK cells via the JNK pathway. Taken together, the protected expression of NKG2D by IL-2/IL-18 provides insight into the mechanism of NKG2D regulation and it also supplied useful information for creating a novel therapeutic approach to treat TGF-beta-secreting cancer cells. (c) 2006 Elsevier Inc. All rights reserved.
- Files in This Item
- There are no files associated with this item.
- Appears in
Collections - 대학 > 기초교양대학 > 기초교양학부 > 1. Journal Articles
- 원격대학원 > 향장미용학과 > 1. Journal Articles
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.