AI Article Synopsis
- Natural killer (NK) cells, crucial for tumor immunity, interact with tumor cells via receptors like DNAM-1, which recognizes the CD155 molecule found in certain cancers, notably hepatocellular carcinoma (HCC).
- Analysis showed elevated soluble CD155 in the blood of HCC patients, linked to advanced disease, while CD155 expression in HCC cells correlated with improved overall survival, indicating a complex relationship.
- Further, CD155 interaction led to reduced DNAM-1 expression in NK cells, which resulted in impaired cytotoxic activity, pointing to mechanisms that allow HCC to escape immune detection.
Article Abstract
Background: Natural killer (NK) cells play a key role in immune surveillance and response to tumors, their function regulated by NK cell receptors and their ligands. The DNAM-1 activating receptor recognizes the CD155 molecule expressed in several tumor cells, such as hepatocellular carcinoma (HCC). This study aims to investigate the role of the DNAM-1/CD155 axis in mediating the NK cell response in patients with HCC.
Methods: Soluble CD155 was measured by ELISA. CD155 expression was sought in HCC cells by immunohistochemistry, qPCR, and flow cytometry. DNAM-1 modulation in NK cells was evaluated in transwell experiments and by a siRNA-mediated knockdown. NK cell functions were examined by direct DNAM-1 triggering.
Results: sCD155 was increased in sera from HCC patients and correlated with the parameters of an advanced disease. The expression of CD155 in HCC showed a positive trend toward better overall survival. DNAM-1 downmodulation was induced by CD155-expressing HCC cells, in agreement with lower DNAM-1 expressions in tumor-infiltrating NK (NK-TIL) cells. DNAM-1-mediated cytotoxicity was defective both in circulating NK cells and in NK-TIL of HCC patients.
Conclusions: We provide evidence of alterations in the DNAM-1/CD155 axis in HCC, suggesting a possible mechanism of tumor resistance to innate immune surveillance.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9406989 | PMC |
| http://dx.doi.org/10.3390/cancers14164060 | DOI Listing |
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