Recognition of Tumor Nidogen-1 by Neutrophil C-Type Lectin Receptors

Ronit Vogt Sionov, Chrystelle Lamagna, Zvi Granot*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

2 Scopus citations


Neutrophil-mediated cytotoxicity toward tumor cells requires cell contact and is mediated by hydrogen peroxide. We have recently shown that cathepsin G expressed on the neutrophil surface interacts with tumor RAGE, and this interaction facilitates neutrophil cytotoxicity. Interruption of the cathepsin G–RAGE interaction led to 50–80% reduction in cytotoxicity, suggesting that additional interactions are also involved. Here we show that blocking antibodies to the C-type lectin receptors (CLRs) Clec4e and Dectin-1, but not those to NKG2D, attenuated murine neutrophil cytotoxicity towards murine tumor cells, suggesting a contributing role for these CLRs in neutrophil recognition of tumor cells. We further observed that the CLRs interact with tumor Nidogen-1 and Hspg2, two sulfated glycoproteins of the basement membrane. Both Nidogen-1 and Hspg2 were found to be expressed on the tumor cell surface. The knockdown of Nidogen-1, but not that of Hspg2, led to reduced susceptibility of the tumor cells to neutrophil cytotoxicity. Altogether, this study suggests a role for CLR–Nidogen-1 interaction in the recognition of tumor cells by neutrophils, and this interaction facilitates neutrophil-mediated killing of the tumor cells.

Original languageAmerican English
Article number908
Issue number4
StatePublished - 15 Apr 2022

Bibliographical note

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© 2022 by the authors. Licensee MDPI, Basel, Switzerland.


  • C-type lectin receptors
  • cancer
  • neutrophils
  • nidogen-1


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