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The combination of the CD38 mAb with an IMiD remarkably enhances NK cell-mediated ADCC by increasing the quantity and activity of NK cells, promoting the tumoricidal activity of macrophages, and enhancing CD38 mAb-mediated ADCP

The mechanism by which CD38 mediated PD-1/PD-L1 blockade resistance likely includes perturbation of adenosine receptor signaling in tumor microenvironment leading to immune modulation (87)

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