Combining NK cells and mAb9.2.27 to combat NG2-dependent and anti-inflammatory signals in glioblastoma

Glioblastoma is a deadly brain cancer with limited treatment options. Targeting chondroitin sulfate proteoglycan 4 (CSPG4, best known as NG2) with the monoclonal antibody mAb9.2.27 and activated natural killer (NK) cells abrogated the tumor growth and prolonged the survival of glioblastoma-bearing a...

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Autores principales: Kmiecik, Justyna, Gras Navarro, Andrea, Poli, Aurelie, Planagumà, Jesús Planagumà, Zimmer, Jacques, Chekenya, Martha
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Landes Bioscience 2014
Materias:
Author's View
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3916357/
https://www.ncbi.nlm.nih.gov/pubmed/24575382
http://dx.doi.org/10.4161/onci.27185
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author Kmiecik, Justyna
Gras Navarro, Andrea
Poli, Aurelie
Planagumà, Jesús Planagumà
Zimmer, Jacques
Chekenya, Martha
author_facet Kmiecik, Justyna
Gras Navarro, Andrea
Poli, Aurelie
Planagumà, Jesús Planagumà
Zimmer, Jacques
Chekenya, Martha
author_sort Kmiecik, Justyna
collection PubMed
description Glioblastoma is a deadly brain cancer with limited treatment options. Targeting chondroitin sulfate proteoglycan 4 (CSPG4, best known as NG2) with the monoclonal antibody mAb9.2.27 and activated natural killer (NK) cells abrogated the tumor growth and prolonged the survival of glioblastoma-bearing animals by favoring the establishment of a pro-inflammatory microenvironment. The combination of NK cells and mAb9.2.27 recruited ED1(+)CCR2(low) macrophages that stimulated ED1(+)ED2(low)MHCII(high) microglial cells to exert robust cytotoxicity. Our findings demonstrate the therapeutic potential of targeting salient tumor associated-antigens.
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spelling pubmed-39163572014-02-26 Combining NK cells and mAb9.2.27 to combat NG2-dependent and anti-inflammatory signals in glioblastoma Kmiecik, Justyna Gras Navarro, Andrea Poli, Aurelie Planagumà, Jesús Planagumà Zimmer, Jacques Chekenya, Martha Oncoimmunology Author's View Glioblastoma is a deadly brain cancer with limited treatment options. Targeting chondroitin sulfate proteoglycan 4 (CSPG4, best known as NG2) with the monoclonal antibody mAb9.2.27 and activated natural killer (NK) cells abrogated the tumor growth and prolonged the survival of glioblastoma-bearing animals by favoring the establishment of a pro-inflammatory microenvironment. The combination of NK cells and mAb9.2.27 recruited ED1(+)CCR2(low) macrophages that stimulated ED1(+)ED2(low)MHCII(high) microglial cells to exert robust cytotoxicity. Our findings demonstrate the therapeutic potential of targeting salient tumor associated-antigens. Landes Bioscience 2014-01-01 /pmc/articles/PMC3916357/ /pubmed/24575382 http://dx.doi.org/10.4161/onci.27185 Text en Copyright © 2014 Landes Bioscience http://creativecommons.org/licenses/by-nc/3.0/ This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.
spellingShingle Author's View
Kmiecik, Justyna
Gras Navarro, Andrea
Poli, Aurelie
Planagumà, Jesús Planagumà
Zimmer, Jacques
Chekenya, Martha
Combining NK cells and mAb9.2.27 to combat NG2-dependent and anti-inflammatory signals in glioblastoma
title Combining NK cells and mAb9.2.27 to combat NG2-dependent and anti-inflammatory signals in glioblastoma
title_full Combining NK cells and mAb9.2.27 to combat NG2-dependent and anti-inflammatory signals in glioblastoma
title_fullStr Combining NK cells and mAb9.2.27 to combat NG2-dependent and anti-inflammatory signals in glioblastoma
title_full_unstemmed Combining NK cells and mAb9.2.27 to combat NG2-dependent and anti-inflammatory signals in glioblastoma
title_short Combining NK cells and mAb9.2.27 to combat NG2-dependent and anti-inflammatory signals in glioblastoma
title_sort combining nk cells and mab9.2.27 to combat ng2-dependent and anti-inflammatory signals in glioblastoma
topic Author's View
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3916357/
https://www.ncbi.nlm.nih.gov/pubmed/24575382
http://dx.doi.org/10.4161/onci.27185
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