IL-2/IL-18 prevent the down-modulation of NKG2D by TGF-β in NK cells via the c-Jun N-terminal kinase (JNK) pathway

Hyunkeun Song; Dae Young Hur; Kyung Eun Kim; Hyunjeong Park; Taesung Kim; Chul woo Kim; Saic Bang; Dae Ho Cho

doi:10.1016/j.cellimm.2006.09.002

IL-2/IL-18 prevent the down-modulation of NKG2D by TGF-β in NK cells via the c-Jun N-terminal kinase (JNK) pathway

Hyunkeun Song, Dae Young Hur, Kyung Eun Kim, Hyunjeong Park, Taesung Kim, Chul woo Kim, Saic Bang, Dae Ho Cho

Department of Life Sciences

Research output: Contribution to journal › Article › peer-review

42 Citations (Scopus)

Abstract

TGF-β is known to play a major role for the reduced NKG2D expression seen in cancer patients. However, the mechanisms for reduced TGF-β-induced down-regulation of NKG2D are unclear. In this study, we observed that IL-2/IL-18 increased the NKG2D expression in the TGF-β 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-β treated human NK cell line. Moreover, the NK cytotoxicity assay showed that the reduced NK cytotoxicity by TGF-β was recovered by IL-2/IL-18 treatment. The results indicate that IL-2/IL-18 strongly prevented the TGF-β-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-β-secreting cancer cells.

Original language	English
Pages (from-to)	39-45
Number of pages	7
Journal	Cellular Immunology
Volume	242
Issue number	1
DOIs	https://doi.org/10.1016/j.cellimm.2006.09.002
Publication status	Published - 2006 Jul

Bibliographical note

Funding Information:
This study was supported by the Korea Science & Engineering Foundation (KOSEF) through the Tumor Immunity Medical Research Center (TIMRC) at Seoul National University College of Medicine and through the Research Center for Women’s Disease (RCWD; SRC program (R11-2005-017-02003-0)) at Sookmyung Women’s University.

Keywords

IL-18
IL-2
NK cells
NKG2D
TGF-β

ASJC Scopus subject areas

Immunology

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.cellimm.2006.09.002

Cite this

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title = "IL-2/IL-18 prevent the down-modulation of NKG2D by TGF-β in NK cells via the c-Jun N-terminal kinase (JNK) pathway",

abstract = "TGF-β is known to play a major role for the reduced NKG2D expression seen in cancer patients. However, the mechanisms for reduced TGF-β-induced down-regulation of NKG2D are unclear. In this study, we observed that IL-2/IL-18 increased the NKG2D expression in the TGF-β 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-β treated human NK cell line. Moreover, the NK cytotoxicity assay showed that the reduced NK cytotoxicity by TGF-β was recovered by IL-2/IL-18 treatment. The results indicate that IL-2/IL-18 strongly prevented the TGF-β-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-β-secreting cancer cells.",

keywords = "IL-18, IL-2, NK cells, NKG2D, TGF-β",

author = "Hyunkeun Song and Hur, {Dae Young} and Kim, {Kyung Eun} and Hyunjeong Park and Taesung Kim and Kim, {Chul woo} and Saic Bang and Cho, {Dae Ho}",

note = "Funding Information: This study was supported by the Korea Science & Engineering Foundation (KOSEF) through the Tumor Immunity Medical Research Center (TIMRC) at Seoul National University College of Medicine and through the Research Center for Women{\textquoteright}s Disease (RCWD; SRC program (R11-2005-017-02003-0)) at Sookmyung Women{\textquoteright}s University. ",

year = "2006",

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AU - Song, Hyunkeun

AU - Hur, Dae Young

AU - Kim, Kyung Eun

AU - Park, Hyunjeong

AU - Kim, Taesung

AU - Kim, Chul woo

AU - Bang, Saic

AU - Cho, Dae Ho

N1 - Funding Information: This study was supported by the Korea Science & Engineering Foundation (KOSEF) through the Tumor Immunity Medical Research Center (TIMRC) at Seoul National University College of Medicine and through the Research Center for Women’s Disease (RCWD; SRC program (R11-2005-017-02003-0)) at Sookmyung Women’s University.

PY - 2006/7

Y1 - 2006/7

N2 - TGF-β is known to play a major role for the reduced NKG2D expression seen in cancer patients. However, the mechanisms for reduced TGF-β-induced down-regulation of NKG2D are unclear. In this study, we observed that IL-2/IL-18 increased the NKG2D expression in the TGF-β 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-β treated human NK cell line. Moreover, the NK cytotoxicity assay showed that the reduced NK cytotoxicity by TGF-β was recovered by IL-2/IL-18 treatment. The results indicate that IL-2/IL-18 strongly prevented the TGF-β-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-β-secreting cancer cells.

AB - TGF-β is known to play a major role for the reduced NKG2D expression seen in cancer patients. However, the mechanisms for reduced TGF-β-induced down-regulation of NKG2D are unclear. In this study, we observed that IL-2/IL-18 increased the NKG2D expression in the TGF-β 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-β treated human NK cell line. Moreover, the NK cytotoxicity assay showed that the reduced NK cytotoxicity by TGF-β was recovered by IL-2/IL-18 treatment. The results indicate that IL-2/IL-18 strongly prevented the TGF-β-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-β-secreting cancer cells.

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IL-2/IL-18 prevent the down-modulation of NKG2D by TGF-β in NK cells via the c-Jun N-terminal kinase (JNK) pathway

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

UN SDGs

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