Fig. 1.

A glycocalyx approach to cancer immunotherapy targeting the sialic acid axis of immune modulation. (A) In sialic acid-overexpressing cancer cells, hypersialylated glycans interact with NK inhibitory receptors, leading to inhibition of NK cell activation. (B) Removal of cell-surface sialic acids by an antibody–sialidase conjugate (T-Sia) abolishes the interaction of sialylated glycans and NK-inhibitory Siglec receptors and increases the binding between NK-activating NKG2D receptor and its ligands, thereby enhancing the tumor cell susceptibility to NK cell-mediated ADCC.