Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2015 Feb 10;7(2):303–310. doi: 10.1080/19420862.2015.1011450

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2015 The Author(s). Published with license by Taylor & Francis Group, LLC

© Kipp Weiskopf and Irving L Weissman

This is an Open Access article distributed under the terms of the Creative Commons Attribution-Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The moral rights of the named author(s) have been asserted.

PMC Copyright notice

Figure 1. — Augmenting macrophage responses to therapeutic antibodies. (A) Tumor-binding antibodies stimulate macrophage phagocytosis via Fcγ receptors (FcγR), which is a major mechanism of action of many therapeutic antibodies. (B) The CD47-SIRPα interaction inhibits maximal antibody-dependent phagocytosis. CD47-blocking therapies (blue antibody) prevent inhibitory signaling from SIRPα to augment macrophage activation. (C) Tumor-binding antibodies with engineered Fc fragments exhibit enhanced binding to Fc receptors and potently stimulate phagocytosis. (D) Bispecific antibodies that have dual specificity for tumor antigens and receptors on macrophages can augment phagocytosis and direct macrophage responses against tumors. “Trifunctional” antibodies have intact Fc fragments that can engage additional Fc receptors as depicted. Antibody-drug conjugates with immunostimulatory properties (not depicted) also deliver activating stimuli to macrophages.