Natural Killer Cell Education Is Associated With a Distinct Glycolytic Profile

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Natural Killer Cell Education Is Associated With a Distinct Glycolytic Profile. / Pfeifer, Caroline; Highton, Andrew J; Peine, Sven; Sauter, Jürgen; Schmidt, Alexander H; Bunders, Madeleine J; Altfeld, Marcus; Körner, Christian.

in: FRONT IMMUNOL, Jahrgang 9, 2018, S. 3020.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ZeitschriftenaufsatzForschungBegutachtung

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@article{4faa23e4712d4cc2b637bebe8e260454,
title = "Natural Killer Cell Education Is Associated With a Distinct Glycolytic Profile",
abstract = "NK cells expressing self-inhibitory receptors display increased functionality compared to NK cells lacking those receptors. The acquisition of functional competence in these particular NK-cell subsets is termed education. Little is known about the underlying mechanisms that lead to the functional differences between educated and uneducated NK cells. An increasing number of studies suggest that cellular metabolism is a determinant of immune cell functions. Thus, alterations in cellular metabolic pathways may play a role in the process of NK-cell education. Here, we compared the glycolytic profile of educated and uneducated primary human NK cells. KIR-educated NK cells showed significantly increased expression levels of the glucose transporter Glut1 in comparison to NKG2A-educated or uneducated NK cells with and without exposure to target cells. Subsequently, the metabolic profile of NK-cell subsets was determined using a Seahorse XF Analyzer. Educated NK cells displayed significantly higher rates of cellular glycolysis than uneducated NK cells even in a resting state. Our results indicate that educated and uneducated NK cells reside in different metabolic states prior to activation. These differences in the ability to utilize glucose may represent an underlying mechanism for the superior functionality of educated NK cells expressing self-inhibitory receptors.",
keywords = "Cell Line, Glucose Transporter Type 1/metabolism, Glycolysis/immunology, Healthy Volunteers, Humans, Immunomagnetic Separation, Killer Cells, Natural/immunology, NK Cell Lectin-Like Receptor Subfamily C/immunology, Primary Cell Culture",
author = "Caroline Pfeifer and Highton, {Andrew J} and Sven Peine and J{\"u}rgen Sauter and Schmidt, {Alexander H} and Bunders, {Madeleine J} and Marcus Altfeld and Christian K{\"o}rner",
year = "2018",
doi = "10.3389/fimmu.2018.03020",
language = "English",
volume = "9",
pages = "3020",
journal = "FRONT IMMUNOL",
issn = "1664-3224",
publisher = "Lausanne : Frontiers Research Foundation",

}

RIS

TY - JOUR

T1 - Natural Killer Cell Education Is Associated With a Distinct Glycolytic Profile

AU - Pfeifer, Caroline

AU - Highton, Andrew J

AU - Peine, Sven

AU - Sauter, Jürgen

AU - Schmidt, Alexander H

AU - Bunders, Madeleine J

AU - Altfeld, Marcus

AU - Körner, Christian

PY - 2018

Y1 - 2018

N2 - NK cells expressing self-inhibitory receptors display increased functionality compared to NK cells lacking those receptors. The acquisition of functional competence in these particular NK-cell subsets is termed education. Little is known about the underlying mechanisms that lead to the functional differences between educated and uneducated NK cells. An increasing number of studies suggest that cellular metabolism is a determinant of immune cell functions. Thus, alterations in cellular metabolic pathways may play a role in the process of NK-cell education. Here, we compared the glycolytic profile of educated and uneducated primary human NK cells. KIR-educated NK cells showed significantly increased expression levels of the glucose transporter Glut1 in comparison to NKG2A-educated or uneducated NK cells with and without exposure to target cells. Subsequently, the metabolic profile of NK-cell subsets was determined using a Seahorse XF Analyzer. Educated NK cells displayed significantly higher rates of cellular glycolysis than uneducated NK cells even in a resting state. Our results indicate that educated and uneducated NK cells reside in different metabolic states prior to activation. These differences in the ability to utilize glucose may represent an underlying mechanism for the superior functionality of educated NK cells expressing self-inhibitory receptors.

AB - NK cells expressing self-inhibitory receptors display increased functionality compared to NK cells lacking those receptors. The acquisition of functional competence in these particular NK-cell subsets is termed education. Little is known about the underlying mechanisms that lead to the functional differences between educated and uneducated NK cells. An increasing number of studies suggest that cellular metabolism is a determinant of immune cell functions. Thus, alterations in cellular metabolic pathways may play a role in the process of NK-cell education. Here, we compared the glycolytic profile of educated and uneducated primary human NK cells. KIR-educated NK cells showed significantly increased expression levels of the glucose transporter Glut1 in comparison to NKG2A-educated or uneducated NK cells with and without exposure to target cells. Subsequently, the metabolic profile of NK-cell subsets was determined using a Seahorse XF Analyzer. Educated NK cells displayed significantly higher rates of cellular glycolysis than uneducated NK cells even in a resting state. Our results indicate that educated and uneducated NK cells reside in different metabolic states prior to activation. These differences in the ability to utilize glucose may represent an underlying mechanism for the superior functionality of educated NK cells expressing self-inhibitory receptors.

KW - Cell Line

KW - Glucose Transporter Type 1/metabolism

KW - Glycolysis/immunology

KW - Healthy Volunteers

KW - Humans

KW - Immunomagnetic Separation

KW - Killer Cells, Natural/immunology

KW - NK Cell Lectin-Like Receptor Subfamily C/immunology

KW - Primary Cell Culture

U2 - 10.3389/fimmu.2018.03020

DO - 10.3389/fimmu.2018.03020

M3 - SCORING: Journal article

C2 - 30619362

VL - 9

SP - 3020

JO - FRONT IMMUNOL

JF - FRONT IMMUNOL

SN - 1664-3224

ER -