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Bimodal CD40/Fas-Dependent Crosstalk between iNKT Cells and Tumor-Associated Macrophages Impairs Prostate Cancer Progression

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Bimodal CD40/Fas-Dependent Crosstalk between iNKT Cells and Tumor-Associated Macrophages Impairs Prostate Cancer Progression. / Cortesi, Filippo; Delfanti, Gloria; Grilli, Andrea; Calcinotto, Arianna; Gorini, Francesca; Pucci, Ferdinando; Lucianò, Roberta; Grioni, Matteo; Recchia, Alessandra; Benigni, Fabio; Briganti, Alberto; Salonia, Andrea; De Palma, Michele; Bicciato, Silvio; Doglioni, Claudio; Bellone, Matteo; Casorati, Giulia; Dellabona, Paolo.

In: CELL REP, Vol. 22, No. 11, 13.03.2018, p. 3006-3020.

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

Harvard

Cortesi, F, Delfanti, G, Grilli, A, Calcinotto, A, Gorini, F, Pucci, F, Lucianò, R, Grioni, M, Recchia, A, Benigni, F, Briganti, A, Salonia, A, De Palma, M, Bicciato, S, Doglioni, C, Bellone, M, Casorati, G & Dellabona, P 2018, 'Bimodal CD40/Fas-Dependent Crosstalk between iNKT Cells and Tumor-Associated Macrophages Impairs Prostate Cancer Progression', CELL REP, vol. 22, no. 11, pp. 3006-3020. https://doi.org/10.1016/j.celrep.2018.02.058

APA

Cortesi, F., Delfanti, G., Grilli, A., Calcinotto, A., Gorini, F., Pucci, F., Lucianò, R., Grioni, M., Recchia, A., Benigni, F., Briganti, A., Salonia, A., De Palma, M., Bicciato, S., Doglioni, C., Bellone, M., Casorati, G., & Dellabona, P. (2018). Bimodal CD40/Fas-Dependent Crosstalk between iNKT Cells and Tumor-Associated Macrophages Impairs Prostate Cancer Progression. CELL REP, 22(11), 3006-3020. https://doi.org/10.1016/j.celrep.2018.02.058

Vancouver

Cortesi F, Delfanti G, Grilli A, Calcinotto A, Gorini F, Pucci F et al. Bimodal CD40/Fas-Dependent Crosstalk between iNKT Cells and Tumor-Associated Macrophages Impairs Prostate Cancer Progression. CELL REP. 2018 Mar 13;22(11):3006-3020. https://doi.org/10.1016/j.celrep.2018.02.058

Bibtex

@article{e0c84302bc454b468f9a8743714bdb6e,
title = "Bimodal CD40/Fas-Dependent Crosstalk between iNKT Cells and Tumor-Associated Macrophages Impairs Prostate Cancer Progression",
abstract = "Heterotypic cellular and molecular interactions in the tumor microenvironment (TME) control cancer progression. Here, we show that CD1d-restricted invariant natural killer (iNKT) cells control prostate cancer (PCa) progression by sculpting the TME. In a mouse PCa model, iNKT cells restrained the pro-angiogenic and immunosuppressive capabilities of tumor-infiltrating immune cells by reducing pro-angiogenic TIE2+, M2-like macrophages (TEMs), and sustaining pro-inflammatory M1-like macrophages. iNKT cells directly contacted macrophages in the PCa stroma, and iNKT cell transfer into tumor-bearing mice abated TEMs, delaying tumor progression. iNKT cells modulated macrophages through the cooperative engagement of CD1d, Fas, and CD40, which promoted selective killing of M2-like and survival of M1-like macrophages. Human PCa aggressiveness associate with reduced intra-tumoral iNKT cells, increased TEMs, and expression of pro-angiogenic genes, underscoring the clinical significance of this crosstalk. Therefore, iNKT cells may control PCa through mechanisms involving differential macrophage modulation, which may be harnessed for therapeutically reprogramming the TME.",
keywords = "Animals, CD40 Antigens/metabolism, Disease Progression, Humans, Macrophages/metabolism, Male, Mice, Natural Killer T-Cells/immunology, Prostatic Neoplasms/genetics",
author = "Filippo Cortesi and Gloria Delfanti and Andrea Grilli and Arianna Calcinotto and Francesca Gorini and Ferdinando Pucci and Roberta Lucian{\`o} and Matteo Grioni and Alessandra Recchia and Fabio Benigni and Alberto Briganti and Andrea Salonia and {De Palma}, Michele and Silvio Bicciato and Claudio Doglioni and Matteo Bellone and Giulia Casorati and Paolo Dellabona",
note = "Copyright {\textcopyright} 2018 The Author(s). Published by Elsevier Inc. All rights reserved.",
year = "2018",
month = mar,
day = "13",
doi = "10.1016/j.celrep.2018.02.058",
language = "English",
volume = "22",
pages = "3006--3020",
journal = "CELL REP",
issn = "2211-1247",
publisher = "Elsevier",
number = "11",

}

RIS

TY - JOUR

T1 - Bimodal CD40/Fas-Dependent Crosstalk between iNKT Cells and Tumor-Associated Macrophages Impairs Prostate Cancer Progression

AU - Cortesi, Filippo

AU - Delfanti, Gloria

AU - Grilli, Andrea

AU - Calcinotto, Arianna

AU - Gorini, Francesca

AU - Pucci, Ferdinando

AU - Lucianò, Roberta

AU - Grioni, Matteo

AU - Recchia, Alessandra

AU - Benigni, Fabio

AU - Briganti, Alberto

AU - Salonia, Andrea

AU - De Palma, Michele

AU - Bicciato, Silvio

AU - Doglioni, Claudio

AU - Bellone, Matteo

AU - Casorati, Giulia

AU - Dellabona, Paolo

N1 - Copyright © 2018 The Author(s). Published by Elsevier Inc. All rights reserved.

PY - 2018/3/13

Y1 - 2018/3/13

N2 - Heterotypic cellular and molecular interactions in the tumor microenvironment (TME) control cancer progression. Here, we show that CD1d-restricted invariant natural killer (iNKT) cells control prostate cancer (PCa) progression by sculpting the TME. In a mouse PCa model, iNKT cells restrained the pro-angiogenic and immunosuppressive capabilities of tumor-infiltrating immune cells by reducing pro-angiogenic TIE2+, M2-like macrophages (TEMs), and sustaining pro-inflammatory M1-like macrophages. iNKT cells directly contacted macrophages in the PCa stroma, and iNKT cell transfer into tumor-bearing mice abated TEMs, delaying tumor progression. iNKT cells modulated macrophages through the cooperative engagement of CD1d, Fas, and CD40, which promoted selective killing of M2-like and survival of M1-like macrophages. Human PCa aggressiveness associate with reduced intra-tumoral iNKT cells, increased TEMs, and expression of pro-angiogenic genes, underscoring the clinical significance of this crosstalk. Therefore, iNKT cells may control PCa through mechanisms involving differential macrophage modulation, which may be harnessed for therapeutically reprogramming the TME.

AB - Heterotypic cellular and molecular interactions in the tumor microenvironment (TME) control cancer progression. Here, we show that CD1d-restricted invariant natural killer (iNKT) cells control prostate cancer (PCa) progression by sculpting the TME. In a mouse PCa model, iNKT cells restrained the pro-angiogenic and immunosuppressive capabilities of tumor-infiltrating immune cells by reducing pro-angiogenic TIE2+, M2-like macrophages (TEMs), and sustaining pro-inflammatory M1-like macrophages. iNKT cells directly contacted macrophages in the PCa stroma, and iNKT cell transfer into tumor-bearing mice abated TEMs, delaying tumor progression. iNKT cells modulated macrophages through the cooperative engagement of CD1d, Fas, and CD40, which promoted selective killing of M2-like and survival of M1-like macrophages. Human PCa aggressiveness associate with reduced intra-tumoral iNKT cells, increased TEMs, and expression of pro-angiogenic genes, underscoring the clinical significance of this crosstalk. Therefore, iNKT cells may control PCa through mechanisms involving differential macrophage modulation, which may be harnessed for therapeutically reprogramming the TME.

KW - Animals

KW - CD40 Antigens/metabolism

KW - Disease Progression

KW - Humans

KW - Macrophages/metabolism

KW - Male

KW - Mice

KW - Natural Killer T-Cells/immunology

KW - Prostatic Neoplasms/genetics

U2 - 10.1016/j.celrep.2018.02.058

DO - 10.1016/j.celrep.2018.02.058

M3 - SCORING: Journal article

C2 - 29539427

VL - 22

SP - 3006

EP - 3020

JO - CELL REP

JF - CELL REP

SN - 2211-1247

IS - 11

ER -