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

Justyna Kmiecik; Andrea Gras Navarro; Aurelie Poli; Jesús Planagumà; Jacques Zimmer; Martha Chekenya

doi:10.4161/onci.27185

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

Justyna Kmiecik
, Andrea Gras Navarro
, Aurelie Poli
, Jesús Planagumà
, Jacques Zimmer
, Martha Chekenya^*

^*Corresponding author for this work

Neuro-Immunology Group

Research output: Contribution to journal › Article › Research › peer-review

26 Citations (Scopus)

Abstract

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 proinflammatory microenvironment. The combination of NK cells and mAb9.2.27 recruited ED1⁺CCR2^low macrophages that stimulated ED1⁺ED2^lowMHCII^high microglial cells to exert robust cytotoxicity. Our findings demonstrate the therapeutic potential of targeting salient tumor associated-antigens.

Original language	English
Article number	e27185
Journal	OncoImmunology
Volume	3
Issue number	1
DOIs	https://doi.org/10.4161/onci.27185
Publication status	Published - 2014

Keywords

CNS immunosurveillance
CSPG4
Glioblastoma
NK cells
Passive immunotherapy

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10.4161/onci.27185

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

abstract = "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 proinflammatory microenvironment. The combination of NK cells and mAb9.2.27 recruited ED1+CCR2low macrophages that stimulated ED1+ED2lowMHCIIhigh microglial cells to exert robust cytotoxicity. Our findings demonstrate the therapeutic potential of targeting salient tumor associated-antigens.",

keywords = "CNS immunosurveillance, CSPG4, Glioblastoma, NK cells, Passive immunotherapy",

author = "Justyna Kmiecik and Navarro, \{Andrea Gras\} and Aurelie Poli and Jes{\'u}s Planagum{\`a} and Jacques Zimmer and Martha Chekenya",

note = "Funding Information: This work was supported by grants from The Bergen Medical Research Foundation, Meltzer Fund, The Norwegian Research Council (FRIFORSK) and The Norwegian Cancer Society.",

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doi = "10.4161/onci.27185",

language = "English",

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T1 - Combining NK cells and mAb9.2.27 to combat NG2-dependent and anti-inflammatory signals in glioblastoma

AU - Kmiecik, Justyna

AU - Navarro, Andrea Gras

AU - Poli, Aurelie

AU - Planagumà, Jesús

AU - Zimmer, Jacques

AU - Chekenya, Martha

N1 - Funding Information: This work was supported by grants from The Bergen Medical Research Foundation, Meltzer Fund, The Norwegian Research Council (FRIFORSK) and The Norwegian Cancer Society.

PY - 2014

Y1 - 2014

N2 - 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 proinflammatory microenvironment. The combination of NK cells and mAb9.2.27 recruited ED1+CCR2low macrophages that stimulated ED1+ED2lowMHCIIhigh microglial cells to exert robust cytotoxicity. Our findings demonstrate the therapeutic potential of targeting salient tumor associated-antigens.

AB - 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 proinflammatory microenvironment. The combination of NK cells and mAb9.2.27 recruited ED1+CCR2low macrophages that stimulated ED1+ED2lowMHCIIhigh microglial cells to exert robust cytotoxicity. Our findings demonstrate the therapeutic potential of targeting salient tumor associated-antigens.

KW - CNS immunosurveillance

KW - CSPG4

KW - Glioblastoma

KW - NK cells

KW - Passive immunotherapy

UR - https://www.scopus.com/pages/publications/84899046831

U2 - 10.4161/onci.27185

DO - 10.4161/onci.27185

M3 - Article

AN - SCOPUS:84899046831

SN - 2162-4011

VL - 3

JO - OncoImmunology

JF - OncoImmunology

IS - 1

M1 - e27185

ER -

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

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Keywords

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