CT47A12 アクチベーター

The functional activity of B7-H6, a protein crucial for natural killer (NK) cell-mediated cytotoxicity against tumor cells, can be influenced by various compounds that enhance the immune response, particularly involving NK cells. Interleukin-2 (IL-2) and Interleukin-15 (IL-15) are cytokines that stimulate NK cell activity, potentially augmenting the immune response mediated by B7-H6 and NKp30 interaction. IL-2 and IL-15 can increase the proliferation and activation of NK cells, thereby enhancing their ability to recognize and kill B7-H6-expressing tumor cells.

Immunomodulatory drugs like Lenalidomide, Thalidomide, and Pomalidomide can also enhance NK cell activity. These compounds can increase the expression of activating receptors on NK cells, thereby enhancing the NK cell response to B7-H6-expressing cells. Proteasome inhibitors like Bortezomib and Heat Shock Protein 90 (HSP90) inhibitors, such as 17-AAG, can induce stress in tumor cells, potentially leading to increased expression of B7-H6, making these cells more susceptible to NK cell-mediated killing.

Histone Deacetylase (HDAC) inhibitors, including Vorinostat, can influence gene expression in tumor cells and may upregulate B7-H6 expression. This upregulation can enhance the visibility of tumor cells to NK cells. Toll-Like Receptor (TLR) agonists, such as Imiquimod, activate the immune system and may also enhance the expression of ligands like B7-H6 on tumor cells.

Interferons, particularly IFN-alpha and IFN-gamma, are critical in enhancing NK cell activity and may upregulate B7-H6 expression on tumor cells, thus facilitating NK cell-mediated recognition and elimination of these cells. Additionally, monoclonal antibodies targeting NKp30 can specifically enhance the interaction between NK cells and B7-H6-expressing cells, boosting the NK cell-mediated immune response.