IL-18 enhances ULBP2 expression through the MAPK pathway in leukemia cells

Hyunkeun Song; Kyung Eun Kim; Daeyoung Hur; Jong Seok Lim; Young Yang; Byung Joo Cho; Cherl hyun Kim; Taesung Kim; Saic Bang; Wang Jae Lee; Hyunjeong Park; Dae Ho Cho

doi:10.1016/j.imlet.2008.07.007

IL-18 enhances ULBP2 expression through the MAPK pathway in leukemia cells

Hyunkeun Song, Kyung Eun Kim, Daeyoung Hur, Jong Seok Lim, Young Yang, Byung Joo Cho, Cherl hyun Kim, Taesung Kim, Saic Bang, Wang Jae Lee, Hyunjeong Park, Dae Ho Cho

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

11 Citations (Scopus)

Abstract

Expression of UL16-binding proteins (ULBPs) has been reported in various cancers, such as leukemia and melanoma, and also in some other cancer cell lines. However, the factors that modulate the expression of ULBPs are not well defined. In this study, we investigated the effects of IL-18 on the expression of NKG2D ligands in leukemia cells. IL-18 treatment increased ULBP2 expression in leukemia cells at the mRNA and protein levels. In addition, PD98059 (an ERK1/2 MAPK inhibitor) and SP600125 (a JNK inhibitor) attenuated IL-18-induced ULBP2 expression in a dose-dependent manner. We observed that ERK1/2 and JNK MAPK phosphorylation increased upon treatment with IL-18. IL-18 elevated CD107a expression in cancer cells and increased the cytotoxic activity of NK cells; therefore, we propose that IL-18 increases the susceptibility of target cells by inducing surface expression of ULBP2. Taken together, these findings suggest that IL-18 may play a critical role in regulating ULBP2 expression via the ERK1/2 and JNK MAPK pathways in leukemia cells.

Original language	English
Pages (from-to)	103-107
Number of pages	5
Journal	Immunology Letters
Volume	120
Issue number	1-2
DOIs	https://doi.org/10.1016/j.imlet.2008.07.007
Publication status	Published - 2008 Sept 30

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 and by Seoul Research and Business Development Program (Seoul R&BD Program (10582)).

Keywords

IL-18
NKG2D
Natural killer cells
Tumor immunity
ULBP

ASJC Scopus subject areas

Immunology and Allergy
Immunology

UN SDGs

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

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10.1016/j.imlet.2008.07.007

Cite this

@article{49b9d94749484c199db2e09a21516de9,

title = "IL-18 enhances ULBP2 expression through the MAPK pathway in leukemia cells",

abstract = "Expression of UL16-binding proteins (ULBPs) has been reported in various cancers, such as leukemia and melanoma, and also in some other cancer cell lines. However, the factors that modulate the expression of ULBPs are not well defined. In this study, we investigated the effects of IL-18 on the expression of NKG2D ligands in leukemia cells. IL-18 treatment increased ULBP2 expression in leukemia cells at the mRNA and protein levels. In addition, PD98059 (an ERK1/2 MAPK inhibitor) and SP600125 (a JNK inhibitor) attenuated IL-18-induced ULBP2 expression in a dose-dependent manner. We observed that ERK1/2 and JNK MAPK phosphorylation increased upon treatment with IL-18. IL-18 elevated CD107a expression in cancer cells and increased the cytotoxic activity of NK cells; therefore, we propose that IL-18 increases the susceptibility of target cells by inducing surface expression of ULBP2. Taken together, these findings suggest that IL-18 may play a critical role in regulating ULBP2 expression via the ERK1/2 and JNK MAPK pathways in leukemia cells.",

keywords = "IL-18, NKG2D, Natural killer cells, Tumor immunity, ULBP",

author = "Hyunkeun Song and Kim, {Kyung Eun} and Daeyoung Hur and Lim, {Jong Seok} and Young Yang and Cho, {Byung Joo} and Kim, {Cherl hyun} and Taesung Kim and Saic Bang and Lee, {Wang Jae} and Hyunjeong Park 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's Disease (RCWD; SRC program (R11-2005-017-02003-0)) at Sookmyung Women's University and by Seoul Research and Business Development Program (Seoul R&BD Program (10582)).",

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doi = "10.1016/j.imlet.2008.07.007",

language = "English",

volume = "120",

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journal = "Immunology Letters",

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TY - JOUR

T1 - IL-18 enhances ULBP2 expression through the MAPK pathway in leukemia cells

AU - Song, Hyunkeun

AU - Kim, Kyung Eun

AU - Hur, Daeyoung

AU - Lim, Jong Seok

AU - Yang, Young

AU - Cho, Byung Joo

AU - Kim, Cherl hyun

AU - Kim, Taesung

AU - Bang, Saic

AU - Lee, Wang Jae

AU - Park, Hyunjeong

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 and by Seoul Research and Business Development Program (Seoul R&BD Program (10582)).

PY - 2008/9/30

Y1 - 2008/9/30

N2 - Expression of UL16-binding proteins (ULBPs) has been reported in various cancers, such as leukemia and melanoma, and also in some other cancer cell lines. However, the factors that modulate the expression of ULBPs are not well defined. In this study, we investigated the effects of IL-18 on the expression of NKG2D ligands in leukemia cells. IL-18 treatment increased ULBP2 expression in leukemia cells at the mRNA and protein levels. In addition, PD98059 (an ERK1/2 MAPK inhibitor) and SP600125 (a JNK inhibitor) attenuated IL-18-induced ULBP2 expression in a dose-dependent manner. We observed that ERK1/2 and JNK MAPK phosphorylation increased upon treatment with IL-18. IL-18 elevated CD107a expression in cancer cells and increased the cytotoxic activity of NK cells; therefore, we propose that IL-18 increases the susceptibility of target cells by inducing surface expression of ULBP2. Taken together, these findings suggest that IL-18 may play a critical role in regulating ULBP2 expression via the ERK1/2 and JNK MAPK pathways in leukemia cells.

AB - Expression of UL16-binding proteins (ULBPs) has been reported in various cancers, such as leukemia and melanoma, and also in some other cancer cell lines. However, the factors that modulate the expression of ULBPs are not well defined. In this study, we investigated the effects of IL-18 on the expression of NKG2D ligands in leukemia cells. IL-18 treatment increased ULBP2 expression in leukemia cells at the mRNA and protein levels. In addition, PD98059 (an ERK1/2 MAPK inhibitor) and SP600125 (a JNK inhibitor) attenuated IL-18-induced ULBP2 expression in a dose-dependent manner. We observed that ERK1/2 and JNK MAPK phosphorylation increased upon treatment with IL-18. IL-18 elevated CD107a expression in cancer cells and increased the cytotoxic activity of NK cells; therefore, we propose that IL-18 increases the susceptibility of target cells by inducing surface expression of ULBP2. Taken together, these findings suggest that IL-18 may play a critical role in regulating ULBP2 expression via the ERK1/2 and JNK MAPK pathways in leukemia cells.

KW - IL-18

KW - NKG2D

KW - Natural killer cells

KW - Tumor immunity

KW - ULBP

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JO - Immunology Letters

JF - Immunology Letters

IS - 1-2

ER -

IL-18 enhances ULBP2 expression through the MAPK pathway in leukemia cells

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

UN SDGs

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