Fusobacterium nucleatum subsp. nucleatum RadD binds Siglec-7 and inhibits NK cell-mediated cancer cell killing

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Fusobacterium nucleatum subsp. nucleatum RadD binds Siglec-7 and inhibits NK cell-mediated cancer cell killing. / Galaski, Johanna; Rishiq, Ahmed; Liu, Mingdong; Bsoul, Reem; Bergson, Almog; Lux, Renate; Bachrach, Gilad; Mandelboim, Ofer.

in: ISCIENCE, Jahrgang 27, Nr. 6, 21.06.2024, S. 110157.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ZeitschriftenaufsatzForschungBegutachtung

Harvard

Galaski, J, Rishiq, A, Liu, M, Bsoul, R, Bergson, A, Lux, R, Bachrach, G & Mandelboim, O 2024, 'Fusobacterium nucleatum subsp. nucleatum RadD binds Siglec-7 and inhibits NK cell-mediated cancer cell killing', ISCIENCE, Jg. 27, Nr. 6, S. 110157. https://doi.org/10.1016/j.isci.2024.110157

APA

Galaski, J., Rishiq, A., Liu, M., Bsoul, R., Bergson, A., Lux, R., Bachrach, G., & Mandelboim, O. (2024). Fusobacterium nucleatum subsp. nucleatum RadD binds Siglec-7 and inhibits NK cell-mediated cancer cell killing. ISCIENCE, 27(6), 110157. https://doi.org/10.1016/j.isci.2024.110157

Vancouver

Bibtex

@article{53f080042235456bbdea37b0236908db,
title = "Fusobacterium nucleatum subsp. nucleatum RadD binds Siglec-7 and inhibits NK cell-mediated cancer cell killing",
abstract = "Fusobacterium nucleatum is an oral commensal bacterium that can colonize extraoral tumor entities, such as colorectal cancer and breast cancer. Recent studies revealed its ability to modulate the immune response in the tumor microenvironment (TME), promoting cancer progression and metastasis. Importantly, F. nucleatum subsp. animalis was shown to bind to Siglec-7 via lipopolysaccharides, leading to a pro-inflammatory profile in human monocyte-derived dendritic cells. In this study, we show that F. nucleatum subsp. nucleatum RadD binds to Siglec-7 on NK cells, thereby inhibiting NK cell-mediated cancer cell killing. We demonstrate that this binding is dependent on arginine residue R124 in Siglec-7. Finally, we determine that this binding is independent of the known interaction of RadD with IgA. Taken together, our findings elucidate the targeting of Siglec-7 by F. nucleatum subsp. nucleatum RadD as a means to modulate the NK cell response and potentially promoting immune evasion and tumor progression.",
author = "Johanna Galaski and Ahmed Rishiq and Mingdong Liu and Reem Bsoul and Almog Bergson and Renate Lux and Gilad Bachrach and Ofer Mandelboim",
note = "{\textcopyright} 2024 The Authors.",
year = "2024",
month = jun,
day = "21",
doi = "10.1016/j.isci.2024.110157",
language = "English",
volume = "27",
pages = "110157",
journal = "ISCIENCE",
issn = "2589-0042",
publisher = "Elsevier Inc.",
number = "6",

}

RIS

TY - JOUR

T1 - Fusobacterium nucleatum subsp. nucleatum RadD binds Siglec-7 and inhibits NK cell-mediated cancer cell killing

AU - Galaski, Johanna

AU - Rishiq, Ahmed

AU - Liu, Mingdong

AU - Bsoul, Reem

AU - Bergson, Almog

AU - Lux, Renate

AU - Bachrach, Gilad

AU - Mandelboim, Ofer

N1 - © 2024 The Authors.

PY - 2024/6/21

Y1 - 2024/6/21

N2 - Fusobacterium nucleatum is an oral commensal bacterium that can colonize extraoral tumor entities, such as colorectal cancer and breast cancer. Recent studies revealed its ability to modulate the immune response in the tumor microenvironment (TME), promoting cancer progression and metastasis. Importantly, F. nucleatum subsp. animalis was shown to bind to Siglec-7 via lipopolysaccharides, leading to a pro-inflammatory profile in human monocyte-derived dendritic cells. In this study, we show that F. nucleatum subsp. nucleatum RadD binds to Siglec-7 on NK cells, thereby inhibiting NK cell-mediated cancer cell killing. We demonstrate that this binding is dependent on arginine residue R124 in Siglec-7. Finally, we determine that this binding is independent of the known interaction of RadD with IgA. Taken together, our findings elucidate the targeting of Siglec-7 by F. nucleatum subsp. nucleatum RadD as a means to modulate the NK cell response and potentially promoting immune evasion and tumor progression.

AB - Fusobacterium nucleatum is an oral commensal bacterium that can colonize extraoral tumor entities, such as colorectal cancer and breast cancer. Recent studies revealed its ability to modulate the immune response in the tumor microenvironment (TME), promoting cancer progression and metastasis. Importantly, F. nucleatum subsp. animalis was shown to bind to Siglec-7 via lipopolysaccharides, leading to a pro-inflammatory profile in human monocyte-derived dendritic cells. In this study, we show that F. nucleatum subsp. nucleatum RadD binds to Siglec-7 on NK cells, thereby inhibiting NK cell-mediated cancer cell killing. We demonstrate that this binding is dependent on arginine residue R124 in Siglec-7. Finally, we determine that this binding is independent of the known interaction of RadD with IgA. Taken together, our findings elucidate the targeting of Siglec-7 by F. nucleatum subsp. nucleatum RadD as a means to modulate the NK cell response and potentially promoting immune evasion and tumor progression.

U2 - 10.1016/j.isci.2024.110157

DO - 10.1016/j.isci.2024.110157

M3 - SCORING: Journal article

C2 - 38952680

VL - 27

SP - 110157

JO - ISCIENCE

JF - ISCIENCE

SN - 2589-0042

IS - 6

ER -