Aberrant expression of SLAMF6 constitutes a targetable immune escape mechanism in acute myeloid leukemia
(2025) In Nature Cancer- Abstract
Immunotherapy has shown limited success in acute myeloid leukemia (AML), indicating an incomplete understanding of the underlying immunoregulatory mechanisms. Here we identify an immune evasion mechanism present in 60% of AML cases, wherein primitive AML cells aberrantly express the lymphoid surface protein SLAMF6 (signaling lymphocyte activation molecule family member 6). Knockout of SLAMF6 in AML cells enables T cell activation and highly efficient killing of leukemia cells in coculture systems, demonstrating that SLAMF6 protects AML cells from recognition and elimination by the immune system in a mode analogous to the programmed cell death protein-ligand (PDL1/PD1) axis. Targeting SLAMF6 with an antibody against the SLAMF6... (More)
Immunotherapy has shown limited success in acute myeloid leukemia (AML), indicating an incomplete understanding of the underlying immunoregulatory mechanisms. Here we identify an immune evasion mechanism present in 60% of AML cases, wherein primitive AML cells aberrantly express the lymphoid surface protein SLAMF6 (signaling lymphocyte activation molecule family member 6). Knockout of SLAMF6 in AML cells enables T cell activation and highly efficient killing of leukemia cells in coculture systems, demonstrating that SLAMF6 protects AML cells from recognition and elimination by the immune system in a mode analogous to the programmed cell death protein-ligand (PDL1/PD1) axis. Targeting SLAMF6 with an antibody against the SLAMF6 dimerization site inhibits the SLAMF6-SLAMF6 interaction and induces T cell activation and killing of AML cells both in vitro and in humanized in vivo models. In conclusion, we show that aberrant expression of SLAMF6 is a common and targetable immune escape mechanism that could pave the way for immunotherapy in AML.
(Less)
- author
- organization
-
- LUCC: Lund University Cancer Centre
- Translational Genomic and Functional Studies of Leukemia (research group)
- Division of Clinical Genetics
- Targeted therapies in leukemia (research group)
- Department of Immunotechnology
- Infect@LU
- LTH Profile Area: Food and Bio
- LU-ATMP: Lund University Advanced Therapy Medicinal Products
- LTH Profile Area: Engineering Health
- SciLifeLab Site@Lund
- Synthetic Immunology (research group)
- publishing date
- 2025-10-03
- type
- Contribution to journal
- publication status
- epub
- subject
- in
- Nature Cancer
- publisher
- Nature Publishing Group
- external identifiers
-
- scopus:105017873246
- pmid:41044242
- ISSN
- 2662-1347
- DOI
- 10.1038/s43018-025-01054-6
- language
- English
- LU publication?
- yes
- additional info
- © 2025. The Author(s).
- id
- 2dd627ae-040a-4b28-a9d0-47438994aef8
- date added to LUP
- 2025-10-06 08:42:43
- date last changed
- 2025-11-29 04:01:13
@article{2dd627ae-040a-4b28-a9d0-47438994aef8,
abstract = {{<p>Immunotherapy has shown limited success in acute myeloid leukemia (AML), indicating an incomplete understanding of the underlying immunoregulatory mechanisms. Here we identify an immune evasion mechanism present in 60% of AML cases, wherein primitive AML cells aberrantly express the lymphoid surface protein SLAMF6 (signaling lymphocyte activation molecule family member 6). Knockout of SLAMF6 in AML cells enables T cell activation and highly efficient killing of leukemia cells in coculture systems, demonstrating that SLAMF6 protects AML cells from recognition and elimination by the immune system in a mode analogous to the programmed cell death protein-ligand (PDL1/PD1) axis. Targeting SLAMF6 with an antibody against the SLAMF6 dimerization site inhibits the SLAMF6-SLAMF6 interaction and induces T cell activation and killing of AML cells both in vitro and in humanized in vivo models. In conclusion, we show that aberrant expression of SLAMF6 is a common and targetable immune escape mechanism that could pave the way for immunotherapy in AML.</p>}},
author = {{Sandén, Carl and Landberg, Niklas and Peña-Martínez, Pablo and Thorsson, Hanna and Daga, Shruti and Puente-Moncada, Noelia and Rodriguez-Zabala, Maria and von Palffy, Sofia and Rissler, Marianne and Lazarevic, Vladimir and Juliusson, Gunnar and Ohlin, Mats and Hyrenius-Wittsten, Axel and Orsmark-Pietras, Christina and Lilljebjörn, Henrik and Ågerstam, Helena and Fioretos, Thoas}},
issn = {{2662-1347}},
language = {{eng}},
month = {{10}},
publisher = {{Nature Publishing Group}},
series = {{Nature Cancer}},
title = {{Aberrant expression of SLAMF6 constitutes a targetable immune escape mechanism in acute myeloid leukemia}},
url = {{http://dx.doi.org/10.1038/s43018-025-01054-6}},
doi = {{10.1038/s43018-025-01054-6}},
year = {{2025}},
}
