Two-layered immune escape in AML is overcome by Fcγ receptor activation and inhibition of PGE2 signaling in NK cells

C Charlotte Rothfuß (1Institute of Molecular Immunology, School of Medicine and Health, Technical University of Munich, Munich, Germany) T Tobias Baumann (1Institute of Molecular Immunology, School of Medicine and Health, Technical University of Munich, Munich, Germany) S Sainitin Donakonda (1Institute of Molecular Immunology, School of Medicine and Health, Technical University of Munich, Munich, Germany) B Bettina Brauchle (2Gene Center, Laboratory for Translational Cancer Immunology, Ludwig-Maximilians-Universität München, Munich, Germany) A Anetta Marcinek (2Gene Center, Laboratory for Translational Cancer Immunology, Ludwig-Maximilians-Universität München, Munich, Germany) C Christian Urban (3Institute of Virology, School of Medicine and Health, Technical University of Munich, Munich, Germany) J Julia Mergner A Anna-Marie Pedde (1Institute of Molecular Immunology, School of Medicine and Health, Technical University of Munich, Munich, Germany) A Anna Hirschberger (1Institute of Molecular Immunology, School of Medicine and Health, Technical University of Munich, Munich, Germany) C Christina Krupka (2Gene Center, Laboratory for Translational Cancer Immunology, Ludwig-Maximilians-Universität München, Munich, Germany) A Anne-Sophie Neumann (4Gene Center, Laboratory for Translational Cancer Immunology, Ludwig-Maximilians-Universität München, Munich, Germany) G Gerulf Hänel (Ludwig Maximilian University Hospital, Munich, Germany) C Camilla Merten (5Institut of Molecular and Clinical Immunology, Otto-von-Guericke-Universität Magdeburg, Magdeburg, Germany) R Rupert Öllinger J Judith S. Hecker T Tanja Bauer (3Institute of Virology, School of Medicine and Health, Technical University of Munich, Munich, Germany) C Christian Schmid K Katharina S. Götze J Jennifer Altomonte (9Department of Internal Medicine II, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany) V Veit Bücklein (Ludwig Maximilian University Hospital, Munich, Germany) R Roland Jacobs (10Department of Rheumatology and Clinical Immunology, Hannover Medical School, Hannover, Germany) R Roland Rad C Corina Dawid (8Food Chemistry and Molecular Sensory Science, Technical University of Munich, Munich, Germany) L Luca Simeoni (5Institut of Molecular and Clinical Immunology, Otto-von-Guericke-Universität Magdeburg, Magdeburg, Germany) B Burkhart Schraven (5Institut of Molecular and Clinical Immunology, Otto-von-Guericke-Universität Magdeburg, Magdeburg, Germany) A Andreas Pichlmair M Marion Subklewe (Ludwig Maximilian University Hospital, Munich, Germany) P Percy A. Knolle J Jan P. Böttcher B Bastian Höchst (1Institute of Molecular Immunology, School of Medicine and Health, Technical University of Munich, Munich, Germany)

Abstract

Abstract Loss of anticancer natural killer (NK) cell function in patients with acute myeloid leukemia (AML) is associated with fatal disease progression and remains poorly understood. Here, we demonstrate that AML blasts isolated from patients rapidly inhibit NK cell function and escape NK cell-mediated killing. Transcriptome analysis of NK cells exposed to AML blasts revealed increased CREM expression and transcriptional activity, indicating enhanced cyclic adenosine monophosphate (cAMP) signaling, confirmed by uniform production of the cAMP-inducing prostanoid prostaglandin E2 (PGE2) by all AML-blast isolates from patients. Phosphoproteome analysis disclosed that PGE2 induced a blockade of lymphocyte-specific protein tyrosine kinase (LCK)–extracellular signal-regulated kinase signaling that is crucial for NK cell activation, indicating a 2-layered escape of AML blasts with low expression of NK cell-activating ligands and inhibition of NK cell signaling. To evaluate the therapeutic potential to target PGE2 inhibition, we combined Fcγ-receptor-mediated activation with the prevention of inhibitory PGE2 signaling. This rescued NK cell function and restored the killing of AML blasts. Thus, we identify the PGE2-LCK signaling axis as the key barrier for NK cell activation in 2-layered immune escape of AML blasts that can be targeted for immune therapy to reconstitute anticancer NK cell immunity in patients with AML.

Article Details

Journal Blood
Volume / Issue Vol. 145, Issue 13
Published March 27, 2025
Pages 1395-1406
ISSN 0006-4971
Publisher Elsevier BV

Journal Info

Blood

Elsevier BV

ISSN: 0006-4971 Health Sciences

Authors (30)

C

Charlotte Rothfuß

1Institute of Molecular Immunology, School of Medicine and Health, Technical University of Munich, Munich, Germany

T

Tobias Baumann

1Institute of Molecular Immunology, School of Medicine and Health, Technical University of Munich, Munich, Germany

S

Sainitin Donakonda

1Institute of Molecular Immunology, School of Medicine and Health, Technical University of Munich, Munich, Germany

B

Bettina Brauchle

2Gene Center, Laboratory for Translational Cancer Immunology, Ludwig-Maximilians-Universität München, Munich, Germany

A

Anetta Marcinek

2Gene Center, Laboratory for Translational Cancer Immunology, Ludwig-Maximilians-Universität München, Munich, Germany

C

Christian Urban

3Institute of Virology, School of Medicine and Health, Technical University of Munich, Munich, Germany

J

Julia Mergner

A

Anna-Marie Pedde

1Institute of Molecular Immunology, School of Medicine and Health, Technical University of Munich, Munich, Germany

A

Anna Hirschberger

1Institute of Molecular Immunology, School of Medicine and Health, Technical University of Munich, Munich, Germany

C

Christina Krupka

2Gene Center, Laboratory for Translational Cancer Immunology, Ludwig-Maximilians-Universität München, Munich, Germany

A

Anne-Sophie Neumann

4Gene Center, Laboratory for Translational Cancer Immunology, Ludwig-Maximilians-Universität München, Munich, Germany

G

Gerulf Hänel

Ludwig Maximilian University Hospital, Munich, Germany

C

Camilla Merten

5Institut of Molecular and Clinical Immunology, Otto-von-Guericke-Universität Magdeburg, Magdeburg, Germany

R

Rupert Öllinger

J

Judith S. Hecker

T

Tanja Bauer

3Institute of Virology, School of Medicine and Health, Technical University of Munich, Munich, Germany

C

Christian Schmid

K

Katharina S. Götze

J

Jennifer Altomonte

9Department of Internal Medicine II, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany

V

Veit Bücklein

Ludwig Maximilian University Hospital, Munich, Germany

R

Roland Jacobs

10Department of Rheumatology and Clinical Immunology, Hannover Medical School, Hannover, Germany

R

Roland Rad

C

Corina Dawid

8Food Chemistry and Molecular Sensory Science, Technical University of Munich, Munich, Germany

L

Luca Simeoni

5Institut of Molecular and Clinical Immunology, Otto-von-Guericke-Universität Magdeburg, Magdeburg, Germany

B

Burkhart Schraven

5Institut of Molecular and Clinical Immunology, Otto-von-Guericke-Universität Magdeburg, Magdeburg, Germany

A

Andreas Pichlmair

M

Marion Subklewe

Ludwig Maximilian University Hospital, Munich, Germany

P

Percy A. Knolle

J

Jan P. Böttcher

B

Bastian Höchst

1Institute of Molecular Immunology, School of Medicine and Health, Technical University of Munich, Munich, Germany