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, Vol. 27, No. 6, 21.06.2024, p. 110157.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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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 -