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Oncoimmunology. 2013 Sep 1;2(9):e25773. Epub 2013 Jul 29.

Improving macrophage responses to therapeutic antibodies by molecular engineering of SIRPα variants.

Author information

  • 1Institute for Stem Cell Biology and Regenerative Medicine; Stanford University School of Medicine; Stanford, CA USA ; Ludwig Center for Cancer Stem Cell Research and Medicine; Stanford University School of Medicine; Stanford, CA USA ; Stanford Cancer Institute; Stanford University School of Medicine; Stanford, CA USA.

Abstract

CD47 transduces inhibitory signals through signal-regulatory protein α (SIRPα), a plasma membrane receptor expressed by macrophages. Many cancers upregulate CD47 to evade immunosurveillance. We have recently engineered SIRPα variants that potently antagonize CD47 for use as anticancer immunotherapeutics. These high-affinity SIRPα variants synergize with antineoplastic antibodies by lowering the threshold for macrophage-mediated destruction of malignant cells.

KEYWORDS:

CD47; SIRPa; antibody; cancer; immune checkpoint; immunotherapy; macrophage; molecular engineering; phagocytosis

PMID:
24319639
PMCID:
PMC3850276
DOI:
10.4161/onci.25773
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