Killer cell immunoglobulin-like receptor 2DL4 is expressed in and suppresses the cell growth of Langerhans cell histiocytosis

被引：10

作者：

Takei, Yusuke ^{[1
]}

Ueshima, Chiyuki ^{[1
]}

Kataoka, Tatsuki R. ^{[1
]}

Hirata, Masahiro ^{[1
]}

Sugimoto, Akihiko ^{[1
]}

Rokutan-Kurata, Mariyo ^{[1
]}

Moriyoshi, Koki ^{[1
,2
]}

Ono, Kazuo ^{[3
]}

Murakami, Ichiro ^{[4
]}

Iwamoto, Sanju ^{[5
]}

Haga, Hironori ^{[1
]}

机构：

[1] Kyoto Univ, Dept Diagnost Pathol, Kyoto, Japan

[2] Kyoto Med Ctr, Dept Diagnost Pathol, Kyoto, Japan

[3] Japan Red Cross Soc, Wakayama Med Ctr, Dept Pathol, Wakayama, Japan

[4] Kochi Univ, Fac Med, Sch Med, Dept Pathol, Nankoku, Kochi, Japan

[5] Showa Univ, Sch Pharm, Div Physiol & Pathol, Dept Pharmacol Toxicol & Therapeut, Tokyo, Japan

来源：

ONCOTARGET | 2017年 / 8卷 / 23期

基金：

日本学术振兴会;

关键词：

KIR2DL4; inhibitory receptor; Langerhans cell histiocytosis; ERK; SHP-2; Pathology Section; IFN-GAMMA PRODUCTION; HUMAN MAST-CELLS; HUMAN NK CELLS; KIR2DL4; CD158D; CUTTING EDGE; PROTEIN; LINE; IDENTIFICATION; ACTIVATION; INHIBITOR;

D O I：

10.18632/oncotarget.16936

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Killer cell immunoglobulin-like receptor (KIR) 2DL4 (CD158d) is a receptor for human leukocyte antigen-G. The function of KIR2DL4 has been reported in human natural killer cell lymphoma and mastocytosis, but not in Langerhans cell histiocytosis (LCH). Herein, we examined the expression and function of KIR2DL4 in LCHs. In pathological specimens, 27 of 36 LCH cases (75.0%) were immunohistochemically positive for KIR2DL4. Its expression was independent of age, gender, location, multior single-system, and the status of BRAFV600E immunostaining. We also confirmed the expression of KIR2DL4 mRNA and protein in the human LCH-like cell lines ELD1 and PRU-1. KIR2DL4 protein was distributed in the membrane and cytoplasm of ELD-1 cells, but only in the cytoplasm of PRU-1 cells. An agonistic antibody against KIR2DL4 reduced phosphorylation of extracellular signal-regulated kinases (ERKs) and suppressed the cell growth of ELD-1 cells in a Src homology region 2 domaincontaining phosphatase-2 dependent manner, but it had no effect in PRU-1 cells. These results suggest that KIR2DL4-mediated ERK suppression is a possible therapeutic target for LCH cells.

引用

页码：36964 / 36972

页数：9

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