Use of TLR agonist and anti-CD47 agent to enhance phagocytosis of cancer cells
AssigneeThe Board of Trustees of the Leland Stanford Junior University
InventorsIrving L. Weissman, Mingye Feng, Jens-Peter Volkmer
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Abstract
Therapeutic and diagnostic methods are provided, which methods relate to the induction of expression of calreticulin on phagocytic cells. Specifically, the methods relate to macrophage-mediated programmed cell removal (PrCR), the methods comprising increasing PrCR by contacting a phagocytic cell with a toll-like receptor (TLR) agonist; or down-regulating PrCR by contacting a phagocytic cell with an inhibitor of Bruton's tyrosine kinase (BTK). In some embodiments, an activator of TLR signaling or a BTK agonist is provided in combination with CD4 7 blockade.
Claims10
A method of enhancing programmed cell removal of living cancer cells, the method comprising:
- contacting a population of phagocytic cells with a btk activating TLR agonist in a dose effective to increase expression of calreticulin on the phagocytic cell surface;
- and with an anti-CD47 antibody that blocks binding of CD47 to SIRPα and comprises an Fc region in a dose effective to increase programmed cell removal of the living cancer cells;
- wherein programmed cell removal of cancer cells by the phagocytic cells is enhanced.
Dependencies are inferred from the claim text.