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Checkpoint blockade in solid tumors and B-cell malignancies, with special consideration of the role of CD200

Authors Gorczynski RM, Zhu F

Received 31 July 2017

Accepted for publication 14 September 2017

Published 13 November 2017 Volume 2017:9 Pages 601—609


Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Dr Antonella D'Anneo

Reginald M Gorczynski,1 Fang Zhu2

1Department of Surgical Research, University Health Network, 2Department of Surgical Research, Institute of Medical Sciences, University of Toronto, Toronto, ON, Canada

Abstract: In the ontogeny of a normal immune response, a series of checkpoints must be overcome to ensure that unwanted and/or harmful self-directed activation responses are avoided. Many of the molecules now known to be active in this overseeing of the evolving immune activation cascade, contributing inhibitory signals to dampen an overexuberant response, belong to the immunoglobulin supergene family. These include members of the CD28/CTLA-4:B7.1/B7.2 receptor/ligand family, PD-1 and PDL-1, CD200 and CD200R, and the more recently described V-domain immunoglobulin suppressor of T-cell activation and its ligand (VSIG-3/IGSF11). Unfortunately, from the point of view of improving immunotargeting of cancer cells, triggering these checkpoint inhibitory signaling pathways, so necessary to maintain self-tolerance, simultaneously acts to prevent effective tumor immunity. The recent development of reagents, predominantly antibodies, to act as checkpoint blockade agents, has had a dramatic effect on human cancer treatment, with a marked reported success for anti-CTLA-4 and PD-1 in particular in clinical trials. This review provides a general overview of the data now available showing the promise of such treatments to our cancer armamentarium and elaborates in depth on the potential promise of what can be regarded as an underappreciated target molecule for checkpoint blockade in chronic lymphocytic leukemia and solid tumors, CD200.

Keywords: checkpoint blockade, immunotherapy, oncology, inhibitory pathways, stimulatory pathways, activated T cells

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