Modulation of the Surface Expression of CD158 Killer Cell Ig-like Receptor by Interleukin-2 and Transforming Growth Factor-beta.
10.3349/ymj.2004.45.3.510
- Author:
Eui Cheol SHIN
1
;
Kyung Seon CHOI
;
Se Jong KIM
;
Jeon Soo SHIN
Author Information
1. Department of Microbiology, Yonsei University College of Medicine, Seoul, Korea. jsshin6203@yumc.yonsei.ac.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
NK cells;
killer cell Ig-like receptor;
IL-2, TGF-beta
- MeSH:
Antineoplastic Agents/*pharmacology;
Cells, Cultured;
Human;
Interferon Type II/pharmacology;
Interleukin-12/pharmacology;
Interleukin-18/pharmacology;
Interleukin-2/*pharmacology;
Killer Cells/cytology/*drug effects/*metabolism;
Receptors, Immunologic/*metabolism;
Support, Non-U.S. Gov't;
Transforming Growth Factor beta/*pharmacology
- From:Yonsei Medical Journal
2004;45(3):510-514
- CountryRepublic of Korea
- Language:English
-
Abstract:
Killer cell Ig-like receptor (KIR) binds to HLA class I molecules on the surface of target cells, and it confers inhibitory signals to NK cells. Although NK cytotoxicity can be affected by the change of the surface expression of KIR on NK cells, the effect of cytokines on the regulation of KIR expression has not been thoroughly investigated. Here in our study, we investigated the effect of several cytokines, including IL-2, TGF-beta, IFN-gamma, IL-12 and IL-18, on the surface expression of CD158 KIR, which binds to HLA-C, by the use of FACS analysis. In the isolated NK cells, IL-2 obviously increased the surface expression of CD158 KIR after 72 hr in vitro culture, and this was evidenced by the increased percentage of CD158+ NK cells and the increased mean fluorescence intensity of CD158 in CD158+ NK cells. In contrast, TGF-beta decreased the surface expression of CD158 KIR after 72 hr culture. However, IFN-gamma, IL-12 and IL-18 did not change the expression of CD158 KIR. The modulated expression of KIR by IL-2 and TGF-beta can be associated with the changed NK-cytotoxic target-discriminating ability of NK cells upon their exposure to IL-2 and TGF-beta.
