SIRPα–CD47 Immune Checkpoint Blockade in Anticancer Therapy

Jan 17, 2018Trends in immunology

Blocking the SIRPα-CD47 Immune Checkpoint in Cancer Treatment

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Abstract

The signal-regulatory protein (SIRP)α-CD47 pathway may serve as a promising therapeutic target in cancer treatment.

Inhibitory immune checkpoint blockade has significantly advanced anticancer therapy over the past decade.
Research has predominantly focused on enhancing adaptive immune functions.
Recent findings suggest that the SIRPα-CD47 pathway is a potential target for improving phagocytosis in innate immune cells.
Key issues for future investigations include exploring additional phagocytic receptor targets to enhance SIRPα-CD47 blockade.
Understanding factors beyond the SIRPα-CD47 checkpoint that influence phagocytosis may improve therapeutic outcomes.
Insights into SIRPα-CD47 blockade could help identify patients who may benefit from this therapy and minimize toxicities.

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Inhibitory immune checkpoint blockade has been one of the most significant advances in anticancer therapy of the past decade. Research so far has largely focused on improving adaptive immune functions, but recent studies have indicated that the signal-regulatory protein (SIRP)α-CD47 pathway, a phagocytosis checkpoint in macrophages and other innate immune cells, may be an interesting therapeutic target. Here, we summarize current knowledge about SIRPα-CD47 blockade, and highlight key issues for future investigations. These include the targeting of prophagocytic receptors (Fc receptors or otherwise) to complement SIRPα-CD47 blockade, the understanding of constraints on phagocytosis other than the SIRPα-CD47 checkpoint and the contribution of immune cells other than macrophages. A better understanding of how SIRPα-CD47 blockade works may aid in identifying patients suitable for this therapy, avoiding potential toxicities and designing optimal combination therapies.

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Abstract

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