Abstract
Tumor immune escape is an important part of tumorigenesis and development. Tumor cells can develop a variety of immunosuppressive mechanisms to combat tumor immunity. Exploring tumor cells that escape immune surveillance through the molecular mechanism of related immunosuppression in-depth is helpful to develop the treatment strategies of targeted tumor immune escape. The latest studies show that CD24 on the surface of tumor cells interacts with Siglec-10 on the surface of immune cells to promote the immune escape of tumor cells. It is necessary to comment on the molecular mechanism of inhibiting the activation of immune cells through the interaction between CD24 on tumor cells and Siglec-10 on immune cells, and a treatment strategy of tumors through targeting CD24 on the surface of tumor cells or Siglec-10 on immune cells.
Highlights
The existence of inhibitory receptors or immune checkpoints avoids the injuries caused by excessive immune response, as tumor cells can up-regulate the corresponding immune checkpoints and their ligands and inhibit the activity of immune cells or induce the apoptosis of immune cells, so as to escape the surveillance of the immune system [1]
CD24/Siglec-10 can inhibit the activation of T cells mediated by T cell receptor (TCR) and promote tumor immune escape
The study results suggest that CD24 mediates the apoptosis of human precursor B cells with the activation of multiple caspases in the pro-B and pre-B stages [87]
Summary
The existence of inhibitory receptors or immune checkpoints avoids the injuries caused by excessive immune response, as tumor cells can up-regulate the corresponding immune checkpoints and their ligands and inhibit the activity of immune cells or induce the apoptosis of immune cells, so as to escape the surveillance of the immune system [1]. Its interaction with sialic-acid-binding Ig-like lectin 10 (Siglec-10) can promote tumor immune escape and is expected to become a new target for tumor therapy [6]. The ITIM region is phosphorylated, blocking Toll-like receptor (TLR)-mediated inflammation and activating a series of intracellular signal pathways to achieve effective immunosuppression and promoting tumor immune escape (Figure 1) [31, 43, 44].
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