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Reactive Neutrophil Responses Dependent on the Receptor Tyrosine Kinase c-MET Limit Cancer Immunotherapy

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Reactive Neutrophil Responses Dependent on the Receptor Tyrosine Kinase c-MET Limit Cancer Immunotherapy. / Glodde, Nicole; Bald, Tobias; van den Boorn-Konijnenberg, Debby; Nakamura, Kyohei; O'Donnell, Jake S; Szczepanski, Sabrina; Brandes, Maria; Eickhoff, Sarah; Das, Indrajit; Shridhar, Naveen; Hinze, Daniel; Rogava, Meri; van der Sluis, Tetje C; Ruotsalainen, Janne J; Gaffal, Evelyn; Landsberg, Jennifer; Ludwig, Kerstin U; Wilhelm, Christoph; Riek-Burchardt, Monika; Müller, Andreas J; Gebhardt, Christoffer; Scolyer, Richard A; Long, Georgina V; Janzen, Viktor; Teng, Michele W L; Kastenmüller, Wolfgang; Mazzone, Massimiliano; Smyth, Mark J; Tüting, Thomas; Hölzel, Michael.

In: IMMUNITY, Vol. 47, No. 4, 17.10.2017, p. 789-802.e9.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Glodde, N, Bald, T, van den Boorn-Konijnenberg, D, Nakamura, K, O'Donnell, JS, Szczepanski, S, Brandes, M, Eickhoff, S, Das, I, Shridhar, N, Hinze, D, Rogava, M, van der Sluis, TC, Ruotsalainen, JJ, Gaffal, E, Landsberg, J, Ludwig, KU, Wilhelm, C, Riek-Burchardt, M, Müller, AJ, Gebhardt, C, Scolyer, RA, Long, GV, Janzen, V, Teng, MWL, Kastenmüller, W, Mazzone, M, Smyth, MJ, Tüting, T & Hölzel, M 2017, 'Reactive Neutrophil Responses Dependent on the Receptor Tyrosine Kinase c-MET Limit Cancer Immunotherapy', IMMUNITY, vol. 47, no. 4, pp. 789-802.e9. https://doi.org/10.1016/j.immuni.2017.09.012

APA

Glodde, N., Bald, T., van den Boorn-Konijnenberg, D., Nakamura, K., O'Donnell, J. S., Szczepanski, S., Brandes, M., Eickhoff, S., Das, I., Shridhar, N., Hinze, D., Rogava, M., van der Sluis, T. C., Ruotsalainen, J. J., Gaffal, E., Landsberg, J., Ludwig, K. U., Wilhelm, C., Riek-Burchardt, M., ... Hölzel, M. (2017). Reactive Neutrophil Responses Dependent on the Receptor Tyrosine Kinase c-MET Limit Cancer Immunotherapy. IMMUNITY, 47(4), 789-802.e9. https://doi.org/10.1016/j.immuni.2017.09.012

Vancouver

Glodde N, Bald T, van den Boorn-Konijnenberg D, Nakamura K, O'Donnell JS, Szczepanski S et al. Reactive Neutrophil Responses Dependent on the Receptor Tyrosine Kinase c-MET Limit Cancer Immunotherapy. IMMUNITY. 2017 Oct 17;47(4):789-802.e9. https://doi.org/10.1016/j.immuni.2017.09.012

Bibtex

@article{e840a95e30874313ba884a1b327df00c,
title = "Reactive Neutrophil Responses Dependent on the Receptor Tyrosine Kinase c-MET Limit Cancer Immunotherapy",
abstract = "Inhibitors of the receptor tyrosine kinase c-MET are currently used in the clinic to target oncogenic signaling in tumor cells. We found that concomitant c-MET inhibition promoted adoptive T cell transfer and checkpoint immunotherapies in murine cancer models by increasing effector T cell infiltration in tumors. This therapeutic effect was independent of tumor cell-intrinsic c-MET dependence. Mechanistically, c-MET inhibition impaired the reactive mobilization and recruitment of neutrophils into tumors and draining lymph nodes in response to cytotoxic immunotherapies. In the absence of c-MET inhibition, neutrophils recruited to T cell-inflamed microenvironments rapidly acquired immunosuppressive properties, restraining T cell expansion and effector functions. In cancer patients, high serum levels of the c-MET ligand HGF correlated with increasing neutrophil counts and poor responses to checkpoint blockade therapies. Our findings reveal a role for the HGF/c-MET pathway in neutrophil recruitment and function and suggest that c-MET inhibitor co-treatment may improve responses to cancer immunotherapy in settings beyond c-MET-dependent tumors.",
keywords = "Animals, Cell Line, Tumor, Cell Proliferation, Gene Expression Profiling, Gene Expression Regulation, Neoplastic, Immunotherapy, Interferon-gamma, Kaplan-Meier Estimate, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Knockout, Mice, Transgenic, Neoplasms, Experimental, Neutrophils, Proto-Oncogene Proteins c-met, Signal Transduction, T-Lymphocytes, Tumor Microenvironment, Journal Article",
author = "Nicole Glodde and Tobias Bald and {van den Boorn-Konijnenberg}, Debby and Kyohei Nakamura and O'Donnell, {Jake S} and Sabrina Szczepanski and Maria Brandes and Sarah Eickhoff and Indrajit Das and Naveen Shridhar and Daniel Hinze and Meri Rogava and {van der Sluis}, {Tetje C} and Ruotsalainen, {Janne J} and Evelyn Gaffal and Jennifer Landsberg and Ludwig, {Kerstin U} and Christoph Wilhelm and Monika Riek-Burchardt and M{\"u}ller, {Andreas J} and Christoffer Gebhardt and Scolyer, {Richard A} and Long, {Georgina V} and Viktor Janzen and Teng, {Michele W L} and Wolfgang Kastenm{\"u}ller and Massimiliano Mazzone and Smyth, {Mark J} and Thomas T{\"u}ting and Michael H{\"o}lzel",
note = "Copyright {\textcopyright} 2017 Elsevier Inc. All rights reserved.",
year = "2017",
month = oct,
day = "17",
doi = "10.1016/j.immuni.2017.09.012",
language = "English",
volume = "47",
pages = "789--802.e9",
journal = "IMMUNITY",
issn = "1074-7613",
publisher = "Cell Press",
number = "4",

}

RIS

TY - JOUR

T1 - Reactive Neutrophil Responses Dependent on the Receptor Tyrosine Kinase c-MET Limit Cancer Immunotherapy

AU - Glodde, Nicole

AU - Bald, Tobias

AU - van den Boorn-Konijnenberg, Debby

AU - Nakamura, Kyohei

AU - O'Donnell, Jake S

AU - Szczepanski, Sabrina

AU - Brandes, Maria

AU - Eickhoff, Sarah

AU - Das, Indrajit

AU - Shridhar, Naveen

AU - Hinze, Daniel

AU - Rogava, Meri

AU - van der Sluis, Tetje C

AU - Ruotsalainen, Janne J

AU - Gaffal, Evelyn

AU - Landsberg, Jennifer

AU - Ludwig, Kerstin U

AU - Wilhelm, Christoph

AU - Riek-Burchardt, Monika

AU - Müller, Andreas J

AU - Gebhardt, Christoffer

AU - Scolyer, Richard A

AU - Long, Georgina V

AU - Janzen, Viktor

AU - Teng, Michele W L

AU - Kastenmüller, Wolfgang

AU - Mazzone, Massimiliano

AU - Smyth, Mark J

AU - Tüting, Thomas

AU - Hölzel, Michael

N1 - Copyright © 2017 Elsevier Inc. All rights reserved.

PY - 2017/10/17

Y1 - 2017/10/17

N2 - Inhibitors of the receptor tyrosine kinase c-MET are currently used in the clinic to target oncogenic signaling in tumor cells. We found that concomitant c-MET inhibition promoted adoptive T cell transfer and checkpoint immunotherapies in murine cancer models by increasing effector T cell infiltration in tumors. This therapeutic effect was independent of tumor cell-intrinsic c-MET dependence. Mechanistically, c-MET inhibition impaired the reactive mobilization and recruitment of neutrophils into tumors and draining lymph nodes in response to cytotoxic immunotherapies. In the absence of c-MET inhibition, neutrophils recruited to T cell-inflamed microenvironments rapidly acquired immunosuppressive properties, restraining T cell expansion and effector functions. In cancer patients, high serum levels of the c-MET ligand HGF correlated with increasing neutrophil counts and poor responses to checkpoint blockade therapies. Our findings reveal a role for the HGF/c-MET pathway in neutrophil recruitment and function and suggest that c-MET inhibitor co-treatment may improve responses to cancer immunotherapy in settings beyond c-MET-dependent tumors.

AB - Inhibitors of the receptor tyrosine kinase c-MET are currently used in the clinic to target oncogenic signaling in tumor cells. We found that concomitant c-MET inhibition promoted adoptive T cell transfer and checkpoint immunotherapies in murine cancer models by increasing effector T cell infiltration in tumors. This therapeutic effect was independent of tumor cell-intrinsic c-MET dependence. Mechanistically, c-MET inhibition impaired the reactive mobilization and recruitment of neutrophils into tumors and draining lymph nodes in response to cytotoxic immunotherapies. In the absence of c-MET inhibition, neutrophils recruited to T cell-inflamed microenvironments rapidly acquired immunosuppressive properties, restraining T cell expansion and effector functions. In cancer patients, high serum levels of the c-MET ligand HGF correlated with increasing neutrophil counts and poor responses to checkpoint blockade therapies. Our findings reveal a role for the HGF/c-MET pathway in neutrophil recruitment and function and suggest that c-MET inhibitor co-treatment may improve responses to cancer immunotherapy in settings beyond c-MET-dependent tumors.

KW - Animals

KW - Cell Line, Tumor

KW - Cell Proliferation

KW - Gene Expression Profiling

KW - Gene Expression Regulation, Neoplastic

KW - Immunotherapy

KW - Interferon-gamma

KW - Kaplan-Meier Estimate

KW - Mice, Inbred BALB C

KW - Mice, Inbred C57BL

KW - Mice, Knockout

KW - Mice, Transgenic

KW - Neoplasms, Experimental

KW - Neutrophils

KW - Proto-Oncogene Proteins c-met

KW - Signal Transduction

KW - T-Lymphocytes

KW - Tumor Microenvironment

KW - Journal Article

U2 - 10.1016/j.immuni.2017.09.012

DO - 10.1016/j.immuni.2017.09.012

M3 - SCORING: Journal article

C2 - 29045907

VL - 47

SP - 789-802.e9

JO - IMMUNITY

JF - IMMUNITY

SN - 1074-7613

IS - 4

ER -