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The Tim-3-galectin-9 Secretory Pathway is Involved in the Immune Escape of Human Acute Myeloid Leukemia Cells

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The Tim-3-galectin-9 Secretory Pathway is Involved in the Immune Escape of Human Acute Myeloid Leukemia Cells. / Gonçalves Silva, Isabel; Yasinska, Inna M; Sakhnevych, Svetlana S; Fiedler, Walter; Wellbrock, Jasmin; Bardelli, Marco; Varani, Luca; Hussain, Rohanah; Siligardi, Giuliano; Ceccone, Giacomo; Berger, Steffen M; Ushkaryov, Yuri A; Gibbs, Bernhard F; Fasler-Kan, Elizaveta; Sumbayev, Vadim V.

in: EBIOMEDICINE, Jahrgang 22, 08.2017, S. 44-57.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Gonçalves Silva, I, Yasinska, IM, Sakhnevych, SS, Fiedler, W, Wellbrock, J, Bardelli, M, Varani, L, Hussain, R, Siligardi, G, Ceccone, G, Berger, SM, Ushkaryov, YA, Gibbs, BF, Fasler-Kan, E & Sumbayev, VV 2017, 'The Tim-3-galectin-9 Secretory Pathway is Involved in the Immune Escape of Human Acute Myeloid Leukemia Cells', EBIOMEDICINE, Jg. 22, S. 44-57. https://doi.org/10.1016/j.ebiom.2017.07.018

APA

Gonçalves Silva, I., Yasinska, I. M., Sakhnevych, S. S., Fiedler, W., Wellbrock, J., Bardelli, M., Varani, L., Hussain, R., Siligardi, G., Ceccone, G., Berger, S. M., Ushkaryov, Y. A., Gibbs, B. F., Fasler-Kan, E., & Sumbayev, V. V. (2017). The Tim-3-galectin-9 Secretory Pathway is Involved in the Immune Escape of Human Acute Myeloid Leukemia Cells. EBIOMEDICINE, 22, 44-57. https://doi.org/10.1016/j.ebiom.2017.07.018

Vancouver

Gonçalves Silva I, Yasinska IM, Sakhnevych SS, Fiedler W, Wellbrock J, Bardelli M et al. The Tim-3-galectin-9 Secretory Pathway is Involved in the Immune Escape of Human Acute Myeloid Leukemia Cells. EBIOMEDICINE. 2017 Aug;22:44-57. https://doi.org/10.1016/j.ebiom.2017.07.018

Bibtex

@article{c0f5a7f76cad47d99dc40f674342941e,
title = "The Tim-3-galectin-9 Secretory Pathway is Involved in the Immune Escape of Human Acute Myeloid Leukemia Cells",
abstract = "Acute myeloid leukemia (AML) is a severe and often fatal systemic malignancy. Malignant cells are capable of escaping host immune surveillance by inactivating cytotoxic lymphoid cells. In this work we discovered a fundamental molecular pathway, which includes ligand-dependent activation of ectopically expressed latrophilin 1 and possibly other G-protein coupled receptors leading to increased translation and exocytosis of the immune receptor Tim-3 and its ligand galectin-9. This occurs in a protein kinase C and mTOR (mammalian target of rapamycin)-dependent manner. Tim-3 participates in galectin-9 secretion and is also released in a free soluble form. Galectin-9 impairs the anti-cancer activity of cytotoxic lymphoid cells including natural killer (NK) cells. Soluble Tim-3 prevents secretion of interleukin-2 (IL-2) required for the activation of cytotoxic lymphoid cells. These results were validated in ex vivo experiments using primary samples from AML patients. This pathway provides reliable targets for both highly specific diagnosis and immune therapy of AML.",
keywords = "Animals, Autocrine Communication, Cell Line, Tumor, Galectins, Hepatitis A Virus Cellular Receptor 2, Humans, Interleukin-2, Jurkat Cells, K562 Cells, Killer Cells, Natural, Leukemia, Myeloid, Acute, Mice, Receptors, G-Protein-Coupled, Receptors, Peptide, Signal Transduction, THP-1 Cells, Journal Article",
author = "{Gon{\c c}alves Silva}, Isabel and Yasinska, {Inna M} and Sakhnevych, {Svetlana S} and Walter Fiedler and Jasmin Wellbrock and Marco Bardelli and Luca Varani and Rohanah Hussain and Giuliano Siligardi and Giacomo Ceccone and Berger, {Steffen M} and Ushkaryov, {Yuri A} and Gibbs, {Bernhard F} and Elizaveta Fasler-Kan and Sumbayev, {Vadim V}",
note = "Copyright {\textcopyright} 2017. Published by Elsevier B.V.",
year = "2017",
month = aug,
doi = "10.1016/j.ebiom.2017.07.018",
language = "English",
volume = "22",
pages = "44--57",
journal = "EBIOMEDICINE",
issn = "2352-3964",
publisher = "Elsevier BV",

}

RIS

TY - JOUR

T1 - The Tim-3-galectin-9 Secretory Pathway is Involved in the Immune Escape of Human Acute Myeloid Leukemia Cells

AU - Gonçalves Silva, Isabel

AU - Yasinska, Inna M

AU - Sakhnevych, Svetlana S

AU - Fiedler, Walter

AU - Wellbrock, Jasmin

AU - Bardelli, Marco

AU - Varani, Luca

AU - Hussain, Rohanah

AU - Siligardi, Giuliano

AU - Ceccone, Giacomo

AU - Berger, Steffen M

AU - Ushkaryov, Yuri A

AU - Gibbs, Bernhard F

AU - Fasler-Kan, Elizaveta

AU - Sumbayev, Vadim V

N1 - Copyright © 2017. Published by Elsevier B.V.

PY - 2017/8

Y1 - 2017/8

N2 - Acute myeloid leukemia (AML) is a severe and often fatal systemic malignancy. Malignant cells are capable of escaping host immune surveillance by inactivating cytotoxic lymphoid cells. In this work we discovered a fundamental molecular pathway, which includes ligand-dependent activation of ectopically expressed latrophilin 1 and possibly other G-protein coupled receptors leading to increased translation and exocytosis of the immune receptor Tim-3 and its ligand galectin-9. This occurs in a protein kinase C and mTOR (mammalian target of rapamycin)-dependent manner. Tim-3 participates in galectin-9 secretion and is also released in a free soluble form. Galectin-9 impairs the anti-cancer activity of cytotoxic lymphoid cells including natural killer (NK) cells. Soluble Tim-3 prevents secretion of interleukin-2 (IL-2) required for the activation of cytotoxic lymphoid cells. These results were validated in ex vivo experiments using primary samples from AML patients. This pathway provides reliable targets for both highly specific diagnosis and immune therapy of AML.

AB - Acute myeloid leukemia (AML) is a severe and often fatal systemic malignancy. Malignant cells are capable of escaping host immune surveillance by inactivating cytotoxic lymphoid cells. In this work we discovered a fundamental molecular pathway, which includes ligand-dependent activation of ectopically expressed latrophilin 1 and possibly other G-protein coupled receptors leading to increased translation and exocytosis of the immune receptor Tim-3 and its ligand galectin-9. This occurs in a protein kinase C and mTOR (mammalian target of rapamycin)-dependent manner. Tim-3 participates in galectin-9 secretion and is also released in a free soluble form. Galectin-9 impairs the anti-cancer activity of cytotoxic lymphoid cells including natural killer (NK) cells. Soluble Tim-3 prevents secretion of interleukin-2 (IL-2) required for the activation of cytotoxic lymphoid cells. These results were validated in ex vivo experiments using primary samples from AML patients. This pathway provides reliable targets for both highly specific diagnosis and immune therapy of AML.

KW - Animals

KW - Autocrine Communication

KW - Cell Line, Tumor

KW - Galectins

KW - Hepatitis A Virus Cellular Receptor 2

KW - Humans

KW - Interleukin-2

KW - Jurkat Cells

KW - K562 Cells

KW - Killer Cells, Natural

KW - Leukemia, Myeloid, Acute

KW - Mice

KW - Receptors, G-Protein-Coupled

KW - Receptors, Peptide

KW - Signal Transduction

KW - THP-1 Cells

KW - Journal Article

U2 - 10.1016/j.ebiom.2017.07.018

DO - 10.1016/j.ebiom.2017.07.018

M3 - SCORING: Journal article

C2 - 28750861

VL - 22

SP - 44

EP - 57

JO - EBIOMEDICINE

JF - EBIOMEDICINE

SN - 2352-3964

ER -