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@ARTICLE{Linder:301275,
author = {A. Linder and D. Nixdorf and N. Kuhl and I. Piseddu and T.
Xu and A. V. Holtermann and G. Kuut and R. Endres and N.
Philipp and V. Bücklein and J. de Graaff and T. Carell and
S. Kobold and R. Kischel and V. Hornung and M. Subklewe$^*$},
title = {{STING} activation improves {T}-cell-engaging immunotherapy
for acute myeloid leukemia.},
journal = {Blood},
volume = {145},
number = {19},
issn = {0006-4971},
address = {Washington, DC},
publisher = {American Society of Hematology},
reportid = {DKFZ-2025-00960},
pages = {2149 - 2160},
year = {2025},
abstract = {T-cell-recruiting bispecific antibodies (BsAbs) are in
clinical development for relapsed/refractory acute myeloid
leukemia (AML). Despite promising results, early clinical
trials have failed to demonstrate durable responses. We
investigated whether activation of the innate immune system
through stimulator of interferon (IFN) genes (STING) can
enhance target cell killing by a BsAb targeting CD33 (CD33
bispecific T-cell engager molecule; AMG 330). Indeed, we
show that cytotoxicity against AML mediated by AMG 330 can
be greatly enhanced when combined with the STING agonist
2',3'-cyclic guanosine monophosphate-adenosine monophosphate
(cGAMP) or diamidobenzimidazole (diABZI). We used in vitro
cytotoxicity assays, immunoblotting, transcriptomic
analyses, and extensive CRISPR-Cas9 knockout experiments to
investigate the enhancing effect of a STING agonist on the
cytotoxicity of AMG 330 against AML. Importantly, we
validated our findings with primary AML cells and in a
xenograft AML model. Mechanistically, in addition to direct
cytotoxic effects of STING activation on AML cells,
activated T cells render AML cells more susceptible to STING
activation through their effector cytokines, IFN-γ and
tumor necrosis factor, resulting in enhanced type I IFN
production and induction of IFN-stimulated genes. This feeds
back to the T cells, leading to a further increase in
effector cytokines and an overall cytotoxic T-cell
phenotype, contributing to the beneficial effect of
cGAMP/diABZI in enhancing AMG 330-mediated lysis. We
established a key role for IFN-γ in AMG 330-mediated
cytotoxicity against AML cells and in rendering AML cells
responsive to STING agonism. Here, we propose to improve the
efficacy of CD33-targeting BsAbs by combining them with a
STING agonist.},
keywords = {Leukemia, Myeloid, Acute: immunology / Leukemia, Myeloid,
Acute: therapy / Leukemia, Myeloid, Acute: pathology /
Humans / Membrane Proteins: agonists / Membrane Proteins:
immunology / Membrane Proteins: genetics / Membrane
Proteins: metabolism / Animals / Mice / Immunotherapy:
methods / T-Lymphocytes: immunology / Antibodies,
Bispecific: pharmacology / Antibodies, Bispecific:
therapeutic use / Nucleotides, Cyclic: pharmacology / Cell
Line, Tumor / Xenograft Model Antitumor Assays / Lymphocyte
Activation / Membrane Proteins (NLM Chemicals) / STING1
protein, human (NLM Chemicals) / Antibodies, Bispecific (NLM
Chemicals) / Nucleotides, Cyclic (NLM Chemicals) / cyclic
guanosine monophosphate-adenosine monophosphate (NLM
Chemicals)},
cin = {MU01},
ddc = {610},
cid = {I:(DE-He78)MU01-20160331},
pnm = {899 - ohne Topic (POF4-899)},
pid = {G:(DE-HGF)POF4-899},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:40009483},
doi = {10.1182/blood.2024026934},
url = {https://inrepo02.dkfz.de/record/301275},
}