A group from Department of Chemical Biology, School of Pharmaceutical Sciences, Peking University, Beijing 100191, China, etc. has reported about enzymatic modulation of Siglec-7 expression on NK cells to enhance NK effector functions for better antitumor therapeutics.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8393205/
The sialic acid-binding immunoglobulin-like lectins (Siglecs) found on immune cells (such as natural killer (NK) and T cells) have been designated as glyco-immune checkpoints.
However, the mechanism of this interaction-dependent suppression of antitumor immunity is not well understood. Authors found that an encounter with NK cells triggered the accumulation of Siglec-7 ligands (sialoglycans) on tumor cells. During the course of monitoring interactions between tumor cells and NK cells, we observed a rapid increase of sialoglycans on tumor cell surface within 2 hours. This remodeling occurs through both the transfer of sialoglycans from NK cells to target tumor cells and the accumulation of de novo synthesized sialoglycans on the tumor cells.
A transplantation of expanded allogeneic NK cells has emerged as a promising strategy for cancer treatment.
By enzymatically creating cis high-affinity sialo glycans on NK cell surfaces with cytidine-5′-monophospho (CMP)-FTMCNeu5Ac and ST6Gal1, significant release of Siglec-7 from NK cell surface to the medium was observed during an immune activation by target cancer cells resulting in the enhancement of the NK effector functions for a better antitumor immunity.
