Blockade of CD47 or SIRPα: a new cancer immunotherapy

Aug 18, 2020Expert opinion on therapeutic targets

Blocking CD47 or SIRPα as a new cancer immunotherapy

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Abstract

Targeting the CD47-SIRPα interaction may enhance cancer immunotherapy.

The CD47-SIRPα signaling axis regulates phagocytosis by macrophages.
Interaction between CD47 on tumor cells and SIRPα on macrophages helps tumors evade immune detection.
Antibodies and other therapies aimed at disrupting the CD47-SIRPα interaction show potential for clinical application.
Current immunotherapeutic strategies targeting this axis face limitations that need addressing.
Future studies may explore new methods to improve interventions targeting the CD47-SIRPα pathway.

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The CD47-Signal regulatory protein α (SIRPα) singling axis acts as a crucial regulator that limits the phagocytic activity of professional phagocytes such as macrophages. Recent studies have demonstrated that the interaction between CD47 on tumor cells and SIRPα on macrophages is implicated in the ability of tumors to evade immunosurveillance. Targeting the CD47-SIRPα interaction is therefore considered to be a promising approach for cancer therapy. Herein, we review some of studies displaying the potential clinical application of antibodies and other modalities that target the CD47-SIRPα interaction. Current limitations of the CD47-SIRPα-targeted immunotherapeutic approaches are also discussed as well as other avenues for future study to improve the current strategies in targeting the CD47-SIRPα signaling axis for cancer immunotherapy.

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Abstract

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