Neuropilin-1: a checkpoint target with unique implications for cancer immunology and immunotherapy

Checkpoint blockade immunotherapy established a new paradigm in cancer treatment: for certain patients curative treatment requires immune reinvigoration. Despite this monumental advance, only 20%–30% of patients achieve an objective response to standard of care immunotherapy, necessitating the consi...

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Main Authors: Chang Liu, Creg J Workman, Dario AA Vignali, Christopher A Chuckran, Tullia C Bruno
Format: Article
Language:English
Published: BMJ Publishing Group 2020-10-01
Series:Journal for ImmunoTherapy of Cancer
Online Access:https://jitc.bmj.com/content/8/2/e000967.full
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author Chang Liu
Creg J Workman
Dario AA Vignali
Christopher A Chuckran
Tullia C Bruno
author_facet Chang Liu
Creg J Workman
Dario AA Vignali
Christopher A Chuckran
Tullia C Bruno
author_sort Chang Liu
collection DOAJ
description Checkpoint blockade immunotherapy established a new paradigm in cancer treatment: for certain patients curative treatment requires immune reinvigoration. Despite this monumental advance, only 20%–30% of patients achieve an objective response to standard of care immunotherapy, necessitating the consideration of alternative targets. Optimal strategies will not only stimulate CD8+ T cells, but concomitantly modulate immunosuppressive cells in the tumor microenvironment (TME), most notably regulatory T cells (Treg cells). In this context, the immunoregulatory receptor Neuropilin-1 (NRP1) is garnering renewed attention as it reinforces intratumoral Treg cell function amidst inflammation in the TME. Loss of NRP1 on Treg cells in mouse models restores antitumor immunity without sacrificing peripheral tolerance. Enrichment of NRP1+ Treg cells is observed in patients across multiple malignancies with cancer, both intratumorally and in peripheral sites. Thus, targeting NRP1 may safely undermine intratumoral Treg cell fitness, permitting enhanced inflammatory responses with existing immunotherapies. Furthermore, NRP1 has been recently found to modulate tumor-specific CD8+ T cell responses. Emerging data suggest that NRP1 restricts CD8+ T cell reinvigoration in response to checkpoint inhibitors, and more importantly, acts as a barrier to the long-term durability of CD8+ T cell-mediated tumor immunosurveillance. These novel and distinct regulatory mechanisms present an exciting therapeutic opportunity. This review will discuss the growing literature on NRP1-mediated immune modulation which provides a strong rationale for categorizing NRP1 as both a key checkpoint in the TME as well as an immunotherapeutic target with promise either alone or in combination with current standard of care therapeutic regimens.
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spelling doaj-art-4c63cc756efa449daf9b583b14e837072025-08-20T02:13:19ZengBMJ Publishing GroupJournal for ImmunoTherapy of Cancer2051-14262020-10-018210.1136/jitc-2020-000967Neuropilin-1: a checkpoint target with unique implications for cancer immunology and immunotherapyChang Liu0Creg J Workman1Dario AA Vignali2Christopher A Chuckran3Tullia C Bruno44 Cancer Immunology and Immunotherapy Program, UPMC Hillman Cancer Center, Pittsburgh, Pennsylvania, USAAff1 grid.21925.3d0000000419369000University of Pittsburgh Pittsburgh PA USA1 Department of Immunology, School of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA4 LUMICKS, Waltham, Massachusetts, USA1University of Pittsburgh, Pittsburgh, PA, USACheckpoint blockade immunotherapy established a new paradigm in cancer treatment: for certain patients curative treatment requires immune reinvigoration. Despite this monumental advance, only 20%–30% of patients achieve an objective response to standard of care immunotherapy, necessitating the consideration of alternative targets. Optimal strategies will not only stimulate CD8+ T cells, but concomitantly modulate immunosuppressive cells in the tumor microenvironment (TME), most notably regulatory T cells (Treg cells). In this context, the immunoregulatory receptor Neuropilin-1 (NRP1) is garnering renewed attention as it reinforces intratumoral Treg cell function amidst inflammation in the TME. Loss of NRP1 on Treg cells in mouse models restores antitumor immunity without sacrificing peripheral tolerance. Enrichment of NRP1+ Treg cells is observed in patients across multiple malignancies with cancer, both intratumorally and in peripheral sites. Thus, targeting NRP1 may safely undermine intratumoral Treg cell fitness, permitting enhanced inflammatory responses with existing immunotherapies. Furthermore, NRP1 has been recently found to modulate tumor-specific CD8+ T cell responses. Emerging data suggest that NRP1 restricts CD8+ T cell reinvigoration in response to checkpoint inhibitors, and more importantly, acts as a barrier to the long-term durability of CD8+ T cell-mediated tumor immunosurveillance. These novel and distinct regulatory mechanisms present an exciting therapeutic opportunity. This review will discuss the growing literature on NRP1-mediated immune modulation which provides a strong rationale for categorizing NRP1 as both a key checkpoint in the TME as well as an immunotherapeutic target with promise either alone or in combination with current standard of care therapeutic regimens.https://jitc.bmj.com/content/8/2/e000967.full
spellingShingle Chang Liu
Creg J Workman
Dario AA Vignali
Christopher A Chuckran
Tullia C Bruno
Neuropilin-1: a checkpoint target with unique implications for cancer immunology and immunotherapy
Journal for ImmunoTherapy of Cancer
title Neuropilin-1: a checkpoint target with unique implications for cancer immunology and immunotherapy
title_full Neuropilin-1: a checkpoint target with unique implications for cancer immunology and immunotherapy
title_fullStr Neuropilin-1: a checkpoint target with unique implications for cancer immunology and immunotherapy
title_full_unstemmed Neuropilin-1: a checkpoint target with unique implications for cancer immunology and immunotherapy
title_short Neuropilin-1: a checkpoint target with unique implications for cancer immunology and immunotherapy
title_sort neuropilin 1 a checkpoint target with unique implications for cancer immunology and immunotherapy
url https://jitc.bmj.com/content/8/2/e000967.full
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