Bimodal CD40/Fas-Dependent Crosstalk between iNKT Cells and Tumor-Associated Macrophages Impairs Prostate Cancer Progression
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...
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| Published in | Cell reports (Cambridge) Vol. 22; no. 11; pp. 3006 - 3020 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
13.03.2018
Elsevier |
| Subjects | |
| Online Access | Get full text |
| ISSN | 2211-1247 2211-1247 |
| DOI | 10.1016/j.celrep.2018.02.058 |
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| 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.
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•iNKT cells remodel the tumor microenvironment of mouse prostate cancer•iNKT cells restrict pro-angiogenic TEMs and sustain pro-inflammatory TAMs•iNKT cells differentially modulate TAMs by cooperative CD1d, CD40, and Fas engagement•Aggressive human prostate cancers contain high TEMs and low iNKT cells
Cortesi et al. provide evidence that iNKT cells contribute to cancer immune surveillance. Due to differential tuning of tumor-associated macrophage populations, iNKT cells remodel the microenvironment of prostate cancer, enforcing a tumor-opposing state that controls tumor progression. |
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| AbstractList | 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. : Cortesi et al. provide evidence that iNKT cells contribute to cancer immune surveillance. Due to differential tuning of tumor-associated macrophage populations, iNKT cells remodel the microenvironment of prostate cancer, enforcing a tumor-opposing state that controls tumor progression. Keywords: iNKT cells, CD1d, macrophage, tumor microenvironment, prostate cancer, immunotherapy, CD40, Fas, angiogenesis 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. [Display omitted] •iNKT cells remodel the tumor microenvironment of mouse prostate cancer•iNKT cells restrict pro-angiogenic TEMs and sustain pro-inflammatory TAMs•iNKT cells differentially modulate TAMs by cooperative CD1d, CD40, and Fas engagement•Aggressive human prostate cancers contain high TEMs and low iNKT cells Cortesi et al. provide evidence that iNKT cells contribute to cancer immune surveillance. Due to differential tuning of tumor-associated macrophage populations, iNKT cells remodel the microenvironment of prostate cancer, enforcing a tumor-opposing state that controls tumor progression. 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.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. 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. |
| Author | Recchia, Alessandra Bellone, Matteo Briganti, Alberto Lucianò, Roberta Doglioni, Claudio Pucci, Ferdinando Bicciato, Silvio Salonia, Andrea Grioni, Matteo Grilli, Andrea Benigni, Fabio Calcinotto, Arianna De Palma, Michele Gorini, Francesca Dellabona, Paolo Casorati, Giulia Delfanti, Gloria Cortesi, Filippo |
| Author_xml | – sequence: 1 givenname: Filippo surname: Cortesi fullname: Cortesi, Filippo organization: Experimental Immunology Unit, Division of Immunology, Transplantation and Infectious Diseases, San Raffaele Scientific Institute, Milan 20123, Italy – sequence: 2 givenname: Gloria surname: Delfanti fullname: Delfanti, Gloria organization: Experimental Immunology Unit, Division of Immunology, Transplantation and Infectious Diseases, San Raffaele Scientific Institute, Milan 20123, Italy – sequence: 3 givenname: Andrea surname: Grilli fullname: Grilli, Andrea organization: Center for Genome Research Department of Life Sciences, University of Modena and Reggio Emilia, Modena, Italy – sequence: 4 givenname: Arianna surname: Calcinotto fullname: Calcinotto, Arianna organization: Cellular Immunology Unit, Division of Immunology, Transplantation and Infectious Diseases, San Raffaele Scientific Institute, Milan 20123, Italy – sequence: 5 givenname: Francesca surname: Gorini fullname: Gorini, Francesca organization: Experimental Immunology Unit, Division of Immunology, Transplantation and Infectious Diseases, San Raffaele Scientific Institute, Milan 20123, Italy – sequence: 6 givenname: Ferdinando surname: Pucci fullname: Pucci, Ferdinando organization: Torque Therapeutics Inc., Cambridge, MA 02142, USA – sequence: 7 givenname: Roberta surname: Lucianò fullname: Lucianò, Roberta organization: Division of Pathology, San Raffaele Scientific Institute, Milan 20123, Italy – sequence: 8 givenname: Matteo surname: Grioni fullname: Grioni, Matteo organization: Cellular Immunology Unit, Division of Immunology, Transplantation and Infectious Diseases, San Raffaele Scientific Institute, Milan 20123, Italy – sequence: 9 givenname: Alessandra surname: Recchia fullname: Recchia, Alessandra organization: Centre for Regenerative Medicine, Department of Life Sciences, University of Modena and Reggio Emilia, Modena, Italy – sequence: 10 givenname: Fabio surname: Benigni fullname: Benigni, Fabio organization: Division of Experimental Oncology/Unit of Urology, URI, IRCCS Ospedale San Raffaele, Milan 20123, Italy – sequence: 11 givenname: Alberto surname: Briganti fullname: Briganti, Alberto organization: Division of Experimental Oncology/Unit of Urology, URI, IRCCS Ospedale San Raffaele, Milan 20123, Italy – sequence: 12 givenname: Andrea surname: Salonia fullname: Salonia, Andrea organization: Division of Experimental Oncology/Unit of Urology, URI, IRCCS Ospedale San Raffaele, Milan 20123, Italy – sequence: 13 givenname: Michele surname: De Palma fullname: De Palma, Michele organization: Swiss Institute for Experimental Cancer Research (ISREC), School of Life Sciences, Ecole Polytechnique Fédérale de Lausanne (EPFL), 1015 Lausanne, Switzerland – sequence: 14 givenname: Silvio surname: Bicciato fullname: Bicciato, Silvio organization: Center for Genome Research Department of Life Sciences, University of Modena and Reggio Emilia, Modena, Italy – sequence: 15 givenname: Claudio surname: Doglioni fullname: Doglioni, Claudio organization: Division of Pathology, San Raffaele Scientific Institute, Milan 20123, Italy – sequence: 16 givenname: Matteo surname: Bellone fullname: Bellone, Matteo email: bellone.matteo@hsr.it organization: Cellular Immunology Unit, Division of Immunology, Transplantation and Infectious Diseases, San Raffaele Scientific Institute, Milan 20123, Italy – sequence: 17 givenname: Giulia surname: Casorati fullname: Casorati, Giulia email: casorati.giulia@hsr.it organization: Experimental Immunology Unit, Division of Immunology, Transplantation and Infectious Diseases, San Raffaele Scientific Institute, Milan 20123, Italy – sequence: 18 givenname: Paolo surname: Dellabona fullname: Dellabona, Paolo email: dellabona.paolo@hsr.it organization: Experimental Immunology Unit, Division of Immunology, Transplantation and Infectious Diseases, San Raffaele Scientific Institute, Milan 20123, Italy |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/29539427$$D View this record in MEDLINE/PubMed |
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| Cites_doi | 10.1084/jem.189.7.1121 10.1016/j.immuni.2012.06.016 10.1084/jem.20020092 10.2183/pjab.91.292 10.4049/jimmunol.1001018 10.1038/nri3175 10.1016/j.smim.2009.10.004 10.1016/j.immuni.2014.06.008 10.1126/science.1252510 10.1111/j.1464-410X.2010.09804.x 10.1182/blood-2009-01-200931 10.1038/ncb3371 10.1158/2326-6066.CIR-13-0104 10.1016/S1471-4906(02)02302-5 10.1016/j.celrep.2011.12.005 10.1016/j.cell.2015.10.025 10.4049/jimmunol.171.10.5140 10.1172/JCI37869 10.1182/blood-2007-05-092866 10.1158/1078-0432.CCR-05-0877 10.4049/jimmunol.167.7.4046 10.1038/bjc.1990.87 10.1038/nri3369 10.1002/1521-4141(200106)31:6<1720::AID-IMMU1720>3.0.CO;2-U 10.1038/nrc.2017.51 10.1126/sciimmunol.aah4081 10.4049/jimmunol.1003748 10.1016/j.immuni.2014.08.017 10.1016/j.cell.2011.02.013 10.1016/j.ccr.2012.02.022 10.1038/srep15651 10.1016/j.immuni.2014.06.010 10.1038/mi.2017.34 10.1016/j.ccell.2016.05.017 10.1038/onc.2013.191 10.1158/1078-0432.CCR-10-2547 10.1073/pnas.92.8.3439 10.1182/blood-2016-11-751065 10.1084/jem.20031462 10.1073/pnas.1113744109 10.1172/JCI36264 10.1038/ni.3047 10.1371/journal.pone.0008646 10.1182/blood-2009-01-198564 10.1084/jem.20021650 10.4049/jimmunol.166.11.6578 10.1371/journal.pone.0011311 10.1200/JCO.2011.38.8819 10.1038/ni.1942 10.1158/1078-0432.CCR-16-0600 |
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| Keywords | prostate cancer CD40 iNKT cells angiogenesis immunotherapy macrophage Fas CD1d tumor microenvironment |
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| References | Comito, Giannoni, Segura, Barcellos-de-Souza, Raspollini, Baroni, Lanciotti, Serni, Chiarugi (bib6) 2014; 33 Hermans, Silk, Gileadi, Salio, Mathew, Ritter, Schmidt, Harris, Old, Cerundolo (bib24) 2003; 171 Murray, Allen, Biswas, Fisher, Gilroy, Goerdt, Gordon, Hamilton, Ivashkiv, Lawrence (bib35) 2014; 41 Lynch, Michelet, Zhang, Brennan, Moseman, Lester, Besra, Vomhof-Dekrey, Tighe, Koay (bib31) 2015; 16 Mantovani, Sozzani, Locati, Allavena, Sica (bib32) 2002; 23 McClinton, Miller, Eremin (bib33) 1990; 61 Metelitsa, Wu, Wang, Yang, Warsi, Asgharzadeh, Groshen, Wilson, Seeger (bib34) 2004; 199 Bellone, Ceccon, Grioni, Jachetti, Calcinotto, Napolitano, Freschi, Casorati, Dellabona (bib4) 2010; 5 Lewis, Harney, Pollard (bib27) 2016; 30 Wingender, Krebs, Beutler, Kronenberg (bib53) 2010; 185 De Palma, Biziato, Petrova (bib10) 2017; 17 Smith, Croca, Waddington, Sofat, Griffin, Nicolaides, Isenberg, Torra, Rahman, Jury (bib45) 2016; 1 Lynch, Nowak, Varghese, Clark, Hogan, Toxavidis, Balk, O’Shea, O’Farrelly, Exley (bib30) 2012; 37 Taniguchi, Harada, Dashtsoodol, Kojo (bib51) 2015; 91 Wang, Sedimbi, Löfbom, Singh, Porcelli, Cardell (bib52) 2018; 11 Noy, Pollard (bib39) 2014; 41 Franklin, Liao, Sarkar, Kim, Bivona, Liu, Pamer, Li (bib15) 2014; 344 Nakagawa, Nagafune, Tazunoki, Ehara, Tomura, Iijima, Motoki, Kamishohara, Seki (bib36) 2001; 166 Dhodapkar, Geller, Chang, Shimizu, Fujii, Dhodapkar, Krasovsky (bib13) 2003; 197 Hayakawa, Takeda, Yagita, Kakuta, Iwakura, Van Kaer, Saiki, Okumura (bib22) 2001; 31 Nonomura, Takayama, Nakayama, Nakai, Kawashima, Mukai, Nagahara, Aozasa, Tsujimura (bib37) 2011; 107 Greenberg, DeMayo, Finegold, Medina, Tilley, Aspinall, Cunha, Donjacour, Matusik, Rosen (bib19) 1995; 92 Cortez-Retamozo, Etzrodt, Newton, Rauch, Chudnovskiy, Berger, Ryan, Iwamoto, Marinelli, Gorbatov (bib7) 2012; 109 Tachibana, Onodera, Tsuruyama, Mori, Nagayama, Hiai, Imamura (bib49) 2005; 11 Lissbrant, Stattin, Wikstrom, Damber, Egevad, Bergh (bib28) 2000; 17 Godfrey, Pellicci, Patel, Kjer-Nielsen, McCluskey, Rossjohn (bib17) 2010; 22 de Lalla, Rinaldi, Montagna, Azzimonti, Bernardo, Sangalli, Paganoni, Maccario, Di Cesare-Merlone, Zecca (bib9) 2011; 186 Lundholm, Hägglöf, Wikberg, Stattin, Egevad, Bergh, Wikström, Palmqvist, Edin (bib29) 2015; 5 Kain, Webb, Anderson, Deng, Holt, Costanzo, Zhao, Self, Teyton, Everett (bib25) 2014; 41 De Santo, Salio, Masri, Lee, Dong, Speak, Porubsky, Booth, Veerapen, Besra (bib11) 2008; 118 Pucci, Venneri, Biziato, Nonis, Moi, Sica, Di Serio, Naldini, De Palma (bib40) 2009; 114 Hanahan, Coussens (bib20) 2012; 21 Squadrito, Pucci, Magri, Moi, Gilfillan, Ranghetti, Casazza, Mazzone, Lyle, Naldini, De Palma (bib47) 2012; 1 Brennan, Brigl, Brenner (bib5) 2013; 13 Shimura, Yang, Ebara, Wheeler, Frolov, Thompson (bib44) 2000; 60 Baer, Squadrito, Laoui, Thompson, Hansen, Kiialainen, Hoves, Ries, Ooi, De Palma (bib2) 2016; 18 Renukaradhya, Khan, Vieira, Du, Gervay-Hague, Brutkiewicz (bib41) 2008; 111 Kitamura, Iwakabe, Yahata, Nishimura, Ohta, Ohmi, Sato, Takeda, Okumura, Van Kaer (bib26) 1999; 189 Tahir, Cheng, Shaulov, Koezuka, Bubley, Wilson, Balk, Exley (bib50) 2001; 167 De Santo, Arscott, Booth, Karydis, Jones, Asher, Salio, Middleton, Cerundolo (bib12) 2010; 11 Exley, Friedlander, Alatrakchi, Vriend, Yue, Sasada, Zeng, Mizukami, Clark, Nemer (bib14) 2017; 23 Nowak, Arredouani, Tun-Kyi, Schmidt-Wolf, Sanda, Balk, Exley (bib38) 2010; 5 Swann, Uldrich, van Dommelen, Sharkey, Murray, Godfrey, Smyth (bib48) 2009; 113 Hayakawa, Takeda, Yagita, Smyth, Van Kaer, Okumura, Saiki (bib23) 2002; 100 Schneiders, de Bruin, van den Eertwegh, Scheper, Leemans, Brakenhoff, Langendijk, Verheul, de Gruijl, Molling, van der Vliet (bib43) 2012; 30 Song, Asgharzadeh, Salo, Engell, Wu, Sposto, Ara, Silverman, DeClerck, Seeger, Metelitsa (bib46) 2009; 119 Hanahan, Weinberg (bib21) 2011; 144 Rigamonti, Capuano, Ricupito, Jachetti, Grioni, Generoso, Freschi, Bellone (bib42) 2011; 17 Crowe, Smyth, Godfrey (bib8) 2002; 196 Abeshouse, Ahn, Akbani, Ally, Amin, Andry, Annala, Aprikian, Armenia, Arora (bib1) 2015; 163 Gorini, Azzimonti, Delfanti, Scarfò, Scielzo, Bertilaccio, Ranghetti, Gulino, Doglioni, Di Napoli (bib18) 2017; 129 Bassiri, Das, Guan, Barrett, Brennan, Banerjee, Wiener, Orange, Brenner, Grupp, Nichols (bib3) 2014; 2 Gabrilovich, Ostrand-Rosenberg, Bronte (bib16) 2012; 12 Wingender (10.1016/j.celrep.2018.02.058_bib53) 2010; 185 Metelitsa (10.1016/j.celrep.2018.02.058_bib34) 2004; 199 Hermans (10.1016/j.celrep.2018.02.058_bib24) 2003; 171 Lynch (10.1016/j.celrep.2018.02.058_bib30) 2012; 37 Lynch (10.1016/j.celrep.2018.02.058_bib31) 2015; 16 Smith (10.1016/j.celrep.2018.02.058_bib45) 2016; 1 Dhodapkar (10.1016/j.celrep.2018.02.058_bib13) 2003; 197 Godfrey (10.1016/j.celrep.2018.02.058_bib17) 2010; 22 Kitamura (10.1016/j.celrep.2018.02.058_bib26) 1999; 189 Gabrilovich (10.1016/j.celrep.2018.02.058_bib16) 2012; 12 Franklin (10.1016/j.celrep.2018.02.058_bib15) 2014; 344 Murray (10.1016/j.celrep.2018.02.058_bib35) 2014; 41 Noy (10.1016/j.celrep.2018.02.058_bib39) 2014; 41 de Lalla (10.1016/j.celrep.2018.02.058_bib9) 2011; 186 Nonomura (10.1016/j.celrep.2018.02.058_bib37) 2011; 107 Brennan (10.1016/j.celrep.2018.02.058_bib5) 2013; 13 Hayakawa (10.1016/j.celrep.2018.02.058_bib23) 2002; 100 Kain (10.1016/j.celrep.2018.02.058_bib25) 2014; 41 Lissbrant (10.1016/j.celrep.2018.02.058_bib28) 2000; 17 Rigamonti (10.1016/j.celrep.2018.02.058_bib42) 2011; 17 McClinton (10.1016/j.celrep.2018.02.058_bib33) 1990; 61 Bassiri (10.1016/j.celrep.2018.02.058_bib3) 2014; 2 Renukaradhya (10.1016/j.celrep.2018.02.058_bib41) 2008; 111 De Santo (10.1016/j.celrep.2018.02.058_bib12) 2010; 11 Cortez-Retamozo (10.1016/j.celrep.2018.02.058_bib7) 2012; 109 Tachibana (10.1016/j.celrep.2018.02.058_bib49) 2005; 11 Hayakawa (10.1016/j.celrep.2018.02.058_bib22) 2001; 31 Hanahan (10.1016/j.celrep.2018.02.058_bib21) 2011; 144 Greenberg (10.1016/j.celrep.2018.02.058_bib19) 1995; 92 Comito (10.1016/j.celrep.2018.02.058_bib6) 2014; 33 Hanahan (10.1016/j.celrep.2018.02.058_bib20) 2012; 21 Gorini (10.1016/j.celrep.2018.02.058_bib18) 2017; 129 Abeshouse (10.1016/j.celrep.2018.02.058_bib1) 2015; 163 Exley (10.1016/j.celrep.2018.02.058_bib14) 2017; 23 Lewis (10.1016/j.celrep.2018.02.058_bib27) 2016; 30 Nowak (10.1016/j.celrep.2018.02.058_bib38) 2010; 5 Baer (10.1016/j.celrep.2018.02.058_bib2) 2016; 18 Mantovani (10.1016/j.celrep.2018.02.058_bib32) 2002; 23 Schneiders (10.1016/j.celrep.2018.02.058_bib43) 2012; 30 De Palma (10.1016/j.celrep.2018.02.058_bib10) 2017; 17 Tahir (10.1016/j.celrep.2018.02.058_bib50) 2001; 167 Shimura (10.1016/j.celrep.2018.02.058_bib44) 2000; 60 Bellone (10.1016/j.celrep.2018.02.058_bib4) 2010; 5 De Santo (10.1016/j.celrep.2018.02.058_bib11) 2008; 118 Song (10.1016/j.celrep.2018.02.058_bib46) 2009; 119 Lundholm (10.1016/j.celrep.2018.02.058_bib29) 2015; 5 Pucci (10.1016/j.celrep.2018.02.058_bib40) 2009; 114 Taniguchi (10.1016/j.celrep.2018.02.058_bib51) 2015; 91 Crowe (10.1016/j.celrep.2018.02.058_bib8) 2002; 196 Wang (10.1016/j.celrep.2018.02.058_bib52) 2018; 11 Nakagawa (10.1016/j.celrep.2018.02.058_bib36) 2001; 166 Squadrito (10.1016/j.celrep.2018.02.058_bib47) 2012; 1 Swann (10.1016/j.celrep.2018.02.058_bib48) 2009; 113 |
| References_xml | – volume: 16 start-page: 85 year: 2015 end-page: 95 ident: bib31 article-title: Regulatory iNKT cells lack expression of the transcription factor PLZF and control the homeostasis of T(reg) cells and macrophages in adipose tissue publication-title: Nat. Immunol. – volume: 30 start-page: 18 year: 2016 end-page: 25 ident: bib27 article-title: The multifaceted role of perivascular macrophages in tumors publication-title: Cancer Cell – volume: 1 start-page: eaah4081 year: 2016 ident: bib45 article-title: Cross-talk between iNKT cells and monocytes triggers an atheroprotective immune response in SLE patients with asymptomatic plaque publication-title: Sci. Immunol. – volume: 17 start-page: 457 year: 2017 end-page: 474 ident: bib10 article-title: Microenvironmental regulation of tumour angiogenesis publication-title: Nat. Rev. Cancer – volume: 144 start-page: 646 year: 2011 end-page: 674 ident: bib21 article-title: Hallmarks of cancer: the next generation publication-title: Cell – volume: 171 start-page: 5140 year: 2003 end-page: 5147 ident: bib24 article-title: NKT cells enhance CD4+ and CD8+ T cell responses to soluble antigen in vivo through direct interaction with dendritic cells publication-title: J. Immunol. – volume: 11 start-page: 1039 year: 2010 end-page: 1046 ident: bib12 article-title: Invariant NKT cells modulate the suppressive activity of IL-10-secreting neutrophils differentiated with serum amyloid A publication-title: Nat. Immunol. – volume: 5 start-page: e8646 year: 2010 ident: bib4 article-title: iNKT cells control mouse spontaneous carcinoma independently of tumor-specific cytotoxic T cells publication-title: PLoS ONE – volume: 41 start-page: 543 year: 2014 end-page: 554 ident: bib25 article-title: The identification of the endogenous ligands of natural killer T cells reveals the presence of mammalian α-linked glycosylceramides publication-title: Immunity – volume: 119 start-page: 1524 year: 2009 end-page: 1536 ident: bib46 article-title: Valpha24-invariant NKT cells mediate antitumor activity via killing of tumor-associated macrophages publication-title: J. Clin. Invest. – volume: 111 start-page: 5637 year: 2008 end-page: 5645 ident: bib41 article-title: Type I NKT cells protect (and type II NKT cells suppress) the host’s innate antitumor immune response to a B-cell lymphoma publication-title: Blood – volume: 41 start-page: 49 year: 2014 end-page: 61 ident: bib39 article-title: Tumor-associated macrophages: from mechanisms to therapy publication-title: Immunity – volume: 37 start-page: 574 year: 2012 end-page: 587 ident: bib30 article-title: Adipose tissue invariant NKT cells protect against diet-induced obesity and metabolic disorder through regulatory cytokine production publication-title: Immunity – volume: 107 start-page: 1918 year: 2011 end-page: 1922 ident: bib37 article-title: Infiltration of tumour-associated macrophages in prostate biopsy specimens is predictive of disease progression after hormonal therapy for prostate cancer publication-title: BJU Int. – volume: 18 start-page: 790 year: 2016 end-page: 802 ident: bib2 article-title: Suppression of microRNA activity amplifies IFN-γ-induced macrophage activation and promotes anti-tumour immunity publication-title: Nat. Cell Biol. – volume: 118 start-page: 4036 year: 2008 end-page: 4048 ident: bib11 article-title: Invariant NKT cells reduce the immunosuppressive activity of influenza A virus-induced myeloid-derived suppressor cells in mice and humans publication-title: J. Clin. Invest. – volume: 186 start-page: 4490 year: 2011 end-page: 4499 ident: bib9 article-title: Invariant NKT cell reconstitution in pediatric leukemia patients given HLA-haploidentical stem cell transplantation defines distinct CD4+ and CD4- subset dynamics and correlates with remission state publication-title: J. Immunol. – volume: 17 start-page: 1012 year: 2011 end-page: 1023 ident: bib42 article-title: Modulators of arginine metabolism do not impact on peripheral T-cell tolerance and disease progression in a model of spontaneous prostate cancer publication-title: Clin. Cancer Res. – volume: 166 start-page: 6578 year: 2001 end-page: 6584 ident: bib36 article-title: Mechanisms of the antimetastatic effect in the liver and of the hepatocyte injury induced by alpha-galactosylceramide in mice publication-title: J. Immunol. – volume: 13 start-page: 101 year: 2013 end-page: 117 ident: bib5 article-title: Invariant natural killer T cells: an innate activation scheme linked to diverse effector functions publication-title: Nat. Rev. Immunol. – volume: 60 start-page: 5857 year: 2000 end-page: 5861 ident: bib44 article-title: Reduced infiltration of tumor-associated macrophages in human prostate cancer: association with cancer progression publication-title: Cancer Res. – volume: 197 start-page: 1667 year: 2003 end-page: 1676 ident: bib13 article-title: A reversible defect in natural killer T cell function characterizes the progression of premalignant to malignant multiple myeloma publication-title: J. Exp. Med. – volume: 5 start-page: e11311 year: 2010 ident: bib38 article-title: Defective NKT cell activation by CD1d+ TRAMP prostate tumor cells is corrected by interleukin-12 with α-galactosylceramide publication-title: PLoS ONE – volume: 12 start-page: 253 year: 2012 end-page: 268 ident: bib16 article-title: Coordinated regulation of myeloid cells by tumours publication-title: Nat. Rev. Immunol. – volume: 23 start-page: 549 year: 2002 end-page: 555 ident: bib32 article-title: Macrophage polarization: tumor-associated macrophages as a paradigm for polarized M2 mononuclear phagocytes publication-title: Trends Immunol. – volume: 2 start-page: 59 year: 2014 end-page: 69 ident: bib3 article-title: iNKT cell cytotoxic responses control T-lymphoma growth in vitro and in vivo publication-title: Cancer Immunol. Res. – volume: 109 start-page: 2491 year: 2012 end-page: 2496 ident: bib7 article-title: Origins of tumor-associated macrophages and neutrophils publication-title: Proc. Natl. Acad. Sci. USA – volume: 21 start-page: 309 year: 2012 end-page: 322 ident: bib20 article-title: Accessories to the crime: functions of cells recruited to the tumor microenvironment publication-title: Cancer Cell – volume: 189 start-page: 1121 year: 1999 end-page: 1128 ident: bib26 article-title: The natural killer T (NKT) cell ligand alpha-galactosylceramide demonstrates its immunopotentiating effect by inducing interleukin (IL)-12 production by dendritic cells and IL-12 receptor expression on NKT cells publication-title: J. Exp. Med. – volume: 41 start-page: 14 year: 2014 end-page: 20 ident: bib35 article-title: Macrophage activation and polarization: nomenclature and experimental guidelines publication-title: Immunity – volume: 91 start-page: 292 year: 2015 end-page: 304 ident: bib51 article-title: Discovery of NKT cells and development of NKT cell-targeted anti-tumor immunotherapy publication-title: Proc. Jpn. Acad., Ser. B, Phys. Biol. Sci. – volume: 1 start-page: 141 year: 2012 end-page: 154 ident: bib47 article-title: miR-511-3p modulates genetic programs of tumor-associated macrophages publication-title: Cell Rep. – volume: 11 start-page: 7322 year: 2005 end-page: 7327 ident: bib49 article-title: Increased intratumor Valpha24-positive natural killer T cells: a prognostic factor for primary colorectal carcinomas publication-title: Clin. Cancer Res. – volume: 33 start-page: 2423 year: 2014 end-page: 2431 ident: bib6 article-title: Cancer-associated fibroblasts and M2-polarized macrophages synergize during prostate carcinoma progression publication-title: Oncogene – volume: 17 start-page: 445 year: 2000 end-page: 451 ident: bib28 article-title: Tumor associated macrophages in human prostate cancer: relation to clinicopathological variables and survival publication-title: Int. J. Oncol. – volume: 185 start-page: 2721 year: 2010 end-page: 2729 ident: bib53 article-title: Antigen-specific cytotoxicity by invariant NKT cells in vivo is CD95/CD178-dependent and is correlated with antigenic potency publication-title: J. Immunol. – volume: 100 start-page: 1728 year: 2002 end-page: 1733 ident: bib23 article-title: IFN-gamma-mediated inhibition of tumor angiogenesis by natural killer T-cell ligand, alpha-galactosylceramide publication-title: Blood – volume: 22 start-page: 61 year: 2010 end-page: 67 ident: bib17 article-title: Antigen recognition by CD1d-restricted NKT T cell receptors publication-title: Semin. Immunol. – volume: 113 start-page: 6382 year: 2009 end-page: 6385 ident: bib48 article-title: Type I natural killer T cells suppress tumors caused by p53 loss in mice publication-title: Blood – volume: 92 start-page: 3439 year: 1995 end-page: 3443 ident: bib19 article-title: Prostate cancer in a transgenic mouse publication-title: Proc. Natl. Acad. Sci. USA – volume: 11 start-page: 131 year: 2018 end-page: 143 ident: bib52 article-title: Unique invariant natural killer T cells promote intestinal polyps by suppressing TH1 immunity and promoting regulatory T cells publication-title: Mucosal Immunol. – volume: 167 start-page: 4046 year: 2001 end-page: 4050 ident: bib50 article-title: Loss of IFN-gamma production by invariant NK T cells in advanced cancer publication-title: J. Immunol. – volume: 344 start-page: 921 year: 2014 end-page: 925 ident: bib15 article-title: The cellular and molecular origin of tumor-associated macrophages publication-title: Science – volume: 61 start-page: 400 year: 1990 end-page: 403 ident: bib33 article-title: An immunohistochemical characterisation of the inflammatory cell infiltrate in benign and malignant prostatic disease publication-title: Br. J. Cancer – volume: 5 start-page: 15651 year: 2015 ident: bib29 article-title: Secreted factors from colorectal and prostate cancer cells skew the immune response in opposite directions publication-title: Sci. Rep. – volume: 23 start-page: 3510 year: 2017 end-page: 3519 ident: bib14 article-title: Adoptive transfer of invariant NKT cells as immunotherapy for advanced melanoma: a phase I clinical trial publication-title: Clin. Cancer Res. – volume: 129 start-page: 3440 year: 2017 end-page: 3451 ident: bib18 article-title: Invariant NKT cells contribute to chronic lymphocytic leukemia surveillance and prognosis publication-title: Blood – volume: 114 start-page: 901 year: 2009 end-page: 914 ident: bib40 article-title: A distinguishing gene signature shared by tumor-infiltrating Tie2-expressing monocytes, blood “resident” monocytes, and embryonic macrophages suggests common functions and developmental relationships publication-title: Blood – volume: 30 start-page: 567 year: 2012 end-page: 570 ident: bib43 article-title: Circulating invariant natural killer T-cell numbers predict outcome in head and neck squamous cell carcinoma: updated analysis with 10-year follow-up publication-title: J. Clin. Oncol. – volume: 199 start-page: 1213 year: 2004 end-page: 1221 ident: bib34 article-title: Natural killer T cells infiltrate neuroblastomas expressing the chemokine CCL2 publication-title: J. Exp. Med. – volume: 163 start-page: 1011 year: 2015 end-page: 1025 ident: bib1 article-title: The molecular taxonomy of primary prostate cancer publication-title: Cell – volume: 196 start-page: 119 year: 2002 end-page: 127 ident: bib8 article-title: A critical role for natural killer T cells in immunosurveillance of methylcholanthrene-induced sarcomas publication-title: J. Exp. Med. – volume: 31 start-page: 1720 year: 2001 end-page: 1727 ident: bib22 article-title: Critical contribution of IFN-gamma and NK cells, but not perforin-mediated cytotoxicity, to anti-metastatic effect of alpha-galactosylceramide publication-title: Eur. J. Immunol. – volume: 189 start-page: 1121 year: 1999 ident: 10.1016/j.celrep.2018.02.058_bib26 article-title: The natural killer T (NKT) cell ligand alpha-galactosylceramide demonstrates its immunopotentiating effect by inducing interleukin (IL)-12 production by dendritic cells and IL-12 receptor expression on NKT cells publication-title: J. Exp. Med. doi: 10.1084/jem.189.7.1121 – volume: 37 start-page: 574 year: 2012 ident: 10.1016/j.celrep.2018.02.058_bib30 article-title: Adipose tissue invariant NKT cells protect against diet-induced obesity and metabolic disorder through regulatory cytokine production publication-title: Immunity doi: 10.1016/j.immuni.2012.06.016 – volume: 196 start-page: 119 year: 2002 ident: 10.1016/j.celrep.2018.02.058_bib8 article-title: A critical role for natural killer T cells in immunosurveillance of methylcholanthrene-induced sarcomas publication-title: J. Exp. Med. doi: 10.1084/jem.20020092 – volume: 91 start-page: 292 year: 2015 ident: 10.1016/j.celrep.2018.02.058_bib51 article-title: Discovery of NKT cells and development of NKT cell-targeted anti-tumor immunotherapy publication-title: Proc. Jpn. Acad., Ser. B, Phys. Biol. Sci. doi: 10.2183/pjab.91.292 – volume: 185 start-page: 2721 year: 2010 ident: 10.1016/j.celrep.2018.02.058_bib53 article-title: Antigen-specific cytotoxicity by invariant NKT cells in vivo is CD95/CD178-dependent and is correlated with antigenic potency publication-title: J. Immunol. doi: 10.4049/jimmunol.1001018 – volume: 12 start-page: 253 year: 2012 ident: 10.1016/j.celrep.2018.02.058_bib16 article-title: Coordinated regulation of myeloid cells by tumours publication-title: Nat. Rev. Immunol. doi: 10.1038/nri3175 – volume: 22 start-page: 61 year: 2010 ident: 10.1016/j.celrep.2018.02.058_bib17 article-title: Antigen recognition by CD1d-restricted NKT T cell receptors publication-title: Semin. Immunol. doi: 10.1016/j.smim.2009.10.004 – volume: 41 start-page: 14 year: 2014 ident: 10.1016/j.celrep.2018.02.058_bib35 article-title: Macrophage activation and polarization: nomenclature and experimental guidelines publication-title: Immunity doi: 10.1016/j.immuni.2014.06.008 – volume: 344 start-page: 921 year: 2014 ident: 10.1016/j.celrep.2018.02.058_bib15 article-title: The cellular and molecular origin of tumor-associated macrophages publication-title: Science doi: 10.1126/science.1252510 – volume: 107 start-page: 1918 year: 2011 ident: 10.1016/j.celrep.2018.02.058_bib37 article-title: Infiltration of tumour-associated macrophages in prostate biopsy specimens is predictive of disease progression after hormonal therapy for prostate cancer publication-title: BJU Int. doi: 10.1111/j.1464-410X.2010.09804.x – volume: 114 start-page: 901 year: 2009 ident: 10.1016/j.celrep.2018.02.058_bib40 article-title: A distinguishing gene signature shared by tumor-infiltrating Tie2-expressing monocytes, blood “resident” monocytes, and embryonic macrophages suggests common functions and developmental relationships publication-title: Blood doi: 10.1182/blood-2009-01-200931 – volume: 18 start-page: 790 year: 2016 ident: 10.1016/j.celrep.2018.02.058_bib2 article-title: Suppression of microRNA activity amplifies IFN-γ-induced macrophage activation and promotes anti-tumour immunity publication-title: Nat. Cell Biol. doi: 10.1038/ncb3371 – volume: 2 start-page: 59 year: 2014 ident: 10.1016/j.celrep.2018.02.058_bib3 article-title: iNKT cell cytotoxic responses control T-lymphoma growth in vitro and in vivo publication-title: Cancer Immunol. Res. doi: 10.1158/2326-6066.CIR-13-0104 – volume: 23 start-page: 549 year: 2002 ident: 10.1016/j.celrep.2018.02.058_bib32 article-title: Macrophage polarization: tumor-associated macrophages as a paradigm for polarized M2 mononuclear phagocytes publication-title: Trends Immunol. doi: 10.1016/S1471-4906(02)02302-5 – volume: 1 start-page: 141 year: 2012 ident: 10.1016/j.celrep.2018.02.058_bib47 article-title: miR-511-3p modulates genetic programs of tumor-associated macrophages publication-title: Cell Rep. doi: 10.1016/j.celrep.2011.12.005 – volume: 163 start-page: 1011 year: 2015 ident: 10.1016/j.celrep.2018.02.058_bib1 article-title: The molecular taxonomy of primary prostate cancer publication-title: Cell doi: 10.1016/j.cell.2015.10.025 – volume: 171 start-page: 5140 year: 2003 ident: 10.1016/j.celrep.2018.02.058_bib24 article-title: NKT cells enhance CD4+ and CD8+ T cell responses to soluble antigen in vivo through direct interaction with dendritic cells publication-title: J. Immunol. doi: 10.4049/jimmunol.171.10.5140 – volume: 119 start-page: 1524 year: 2009 ident: 10.1016/j.celrep.2018.02.058_bib46 article-title: Valpha24-invariant NKT cells mediate antitumor activity via killing of tumor-associated macrophages publication-title: J. Clin. Invest. doi: 10.1172/JCI37869 – volume: 111 start-page: 5637 year: 2008 ident: 10.1016/j.celrep.2018.02.058_bib41 article-title: Type I NKT cells protect (and type II NKT cells suppress) the host’s innate antitumor immune response to a B-cell lymphoma publication-title: Blood doi: 10.1182/blood-2007-05-092866 – volume: 11 start-page: 7322 year: 2005 ident: 10.1016/j.celrep.2018.02.058_bib49 article-title: Increased intratumor Valpha24-positive natural killer T cells: a prognostic factor for primary colorectal carcinomas publication-title: Clin. Cancer Res. doi: 10.1158/1078-0432.CCR-05-0877 – volume: 167 start-page: 4046 year: 2001 ident: 10.1016/j.celrep.2018.02.058_bib50 article-title: Loss of IFN-gamma production by invariant NK T cells in advanced cancer publication-title: J. Immunol. doi: 10.4049/jimmunol.167.7.4046 – volume: 61 start-page: 400 year: 1990 ident: 10.1016/j.celrep.2018.02.058_bib33 article-title: An immunohistochemical characterisation of the inflammatory cell infiltrate in benign and malignant prostatic disease publication-title: Br. J. Cancer doi: 10.1038/bjc.1990.87 – volume: 13 start-page: 101 year: 2013 ident: 10.1016/j.celrep.2018.02.058_bib5 article-title: Invariant natural killer T cells: an innate activation scheme linked to diverse effector functions publication-title: Nat. Rev. Immunol. doi: 10.1038/nri3369 – volume: 17 start-page: 445 year: 2000 ident: 10.1016/j.celrep.2018.02.058_bib28 article-title: Tumor associated macrophages in human prostate cancer: relation to clinicopathological variables and survival publication-title: Int. J. Oncol. – volume: 31 start-page: 1720 year: 2001 ident: 10.1016/j.celrep.2018.02.058_bib22 article-title: Critical contribution of IFN-gamma and NK cells, but not perforin-mediated cytotoxicity, to anti-metastatic effect of alpha-galactosylceramide publication-title: Eur. J. Immunol. doi: 10.1002/1521-4141(200106)31:6<1720::AID-IMMU1720>3.0.CO;2-U – volume: 17 start-page: 457 year: 2017 ident: 10.1016/j.celrep.2018.02.058_bib10 article-title: Microenvironmental regulation of tumour angiogenesis publication-title: Nat. Rev. Cancer doi: 10.1038/nrc.2017.51 – volume: 1 start-page: eaah4081 year: 2016 ident: 10.1016/j.celrep.2018.02.058_bib45 article-title: Cross-talk between iNKT cells and monocytes triggers an atheroprotective immune response in SLE patients with asymptomatic plaque publication-title: Sci. Immunol. doi: 10.1126/sciimmunol.aah4081 – volume: 186 start-page: 4490 year: 2011 ident: 10.1016/j.celrep.2018.02.058_bib9 article-title: Invariant NKT cell reconstitution in pediatric leukemia patients given HLA-haploidentical stem cell transplantation defines distinct CD4+ and CD4- subset dynamics and correlates with remission state publication-title: J. Immunol. doi: 10.4049/jimmunol.1003748 – volume: 41 start-page: 543 year: 2014 ident: 10.1016/j.celrep.2018.02.058_bib25 article-title: The identification of the endogenous ligands of natural killer T cells reveals the presence of mammalian α-linked glycosylceramides publication-title: Immunity doi: 10.1016/j.immuni.2014.08.017 – volume: 100 start-page: 1728 year: 2002 ident: 10.1016/j.celrep.2018.02.058_bib23 article-title: IFN-gamma-mediated inhibition of tumor angiogenesis by natural killer T-cell ligand, alpha-galactosylceramide publication-title: Blood – volume: 60 start-page: 5857 year: 2000 ident: 10.1016/j.celrep.2018.02.058_bib44 article-title: Reduced infiltration of tumor-associated macrophages in human prostate cancer: association with cancer progression publication-title: Cancer Res. – volume: 144 start-page: 646 year: 2011 ident: 10.1016/j.celrep.2018.02.058_bib21 article-title: Hallmarks of cancer: the next generation publication-title: Cell doi: 10.1016/j.cell.2011.02.013 – volume: 21 start-page: 309 year: 2012 ident: 10.1016/j.celrep.2018.02.058_bib20 article-title: Accessories to the crime: functions of cells recruited to the tumor microenvironment publication-title: Cancer Cell doi: 10.1016/j.ccr.2012.02.022 – volume: 5 start-page: 15651 year: 2015 ident: 10.1016/j.celrep.2018.02.058_bib29 article-title: Secreted factors from colorectal and prostate cancer cells skew the immune response in opposite directions publication-title: Sci. Rep. doi: 10.1038/srep15651 – volume: 41 start-page: 49 year: 2014 ident: 10.1016/j.celrep.2018.02.058_bib39 article-title: Tumor-associated macrophages: from mechanisms to therapy publication-title: Immunity doi: 10.1016/j.immuni.2014.06.010 – volume: 11 start-page: 131 year: 2018 ident: 10.1016/j.celrep.2018.02.058_bib52 article-title: Unique invariant natural killer T cells promote intestinal polyps by suppressing TH1 immunity and promoting regulatory T cells publication-title: Mucosal Immunol. doi: 10.1038/mi.2017.34 – volume: 30 start-page: 18 year: 2016 ident: 10.1016/j.celrep.2018.02.058_bib27 article-title: The multifaceted role of perivascular macrophages in tumors publication-title: Cancer Cell doi: 10.1016/j.ccell.2016.05.017 – volume: 33 start-page: 2423 year: 2014 ident: 10.1016/j.celrep.2018.02.058_bib6 article-title: Cancer-associated fibroblasts and M2-polarized macrophages synergize during prostate carcinoma progression publication-title: Oncogene doi: 10.1038/onc.2013.191 – volume: 17 start-page: 1012 year: 2011 ident: 10.1016/j.celrep.2018.02.058_bib42 article-title: Modulators of arginine metabolism do not impact on peripheral T-cell tolerance and disease progression in a model of spontaneous prostate cancer publication-title: Clin. Cancer Res. doi: 10.1158/1078-0432.CCR-10-2547 – volume: 92 start-page: 3439 year: 1995 ident: 10.1016/j.celrep.2018.02.058_bib19 article-title: Prostate cancer in a transgenic mouse publication-title: Proc. Natl. Acad. Sci. USA doi: 10.1073/pnas.92.8.3439 – volume: 129 start-page: 3440 year: 2017 ident: 10.1016/j.celrep.2018.02.058_bib18 article-title: Invariant NKT cells contribute to chronic lymphocytic leukemia surveillance and prognosis publication-title: Blood doi: 10.1182/blood-2016-11-751065 – volume: 199 start-page: 1213 year: 2004 ident: 10.1016/j.celrep.2018.02.058_bib34 article-title: Natural killer T cells infiltrate neuroblastomas expressing the chemokine CCL2 publication-title: J. Exp. Med. doi: 10.1084/jem.20031462 – volume: 109 start-page: 2491 year: 2012 ident: 10.1016/j.celrep.2018.02.058_bib7 article-title: Origins of tumor-associated macrophages and neutrophils publication-title: Proc. Natl. Acad. Sci. USA doi: 10.1073/pnas.1113744109 – volume: 118 start-page: 4036 year: 2008 ident: 10.1016/j.celrep.2018.02.058_bib11 article-title: Invariant NKT cells reduce the immunosuppressive activity of influenza A virus-induced myeloid-derived suppressor cells in mice and humans publication-title: J. Clin. Invest. doi: 10.1172/JCI36264 – volume: 16 start-page: 85 year: 2015 ident: 10.1016/j.celrep.2018.02.058_bib31 article-title: Regulatory iNKT cells lack expression of the transcription factor PLZF and control the homeostasis of T(reg) cells and macrophages in adipose tissue publication-title: Nat. Immunol. doi: 10.1038/ni.3047 – volume: 5 start-page: e8646 year: 2010 ident: 10.1016/j.celrep.2018.02.058_bib4 article-title: iNKT cells control mouse spontaneous carcinoma independently of tumor-specific cytotoxic T cells publication-title: PLoS ONE doi: 10.1371/journal.pone.0008646 – volume: 113 start-page: 6382 year: 2009 ident: 10.1016/j.celrep.2018.02.058_bib48 article-title: Type I natural killer T cells suppress tumors caused by p53 loss in mice publication-title: Blood doi: 10.1182/blood-2009-01-198564 – volume: 197 start-page: 1667 year: 2003 ident: 10.1016/j.celrep.2018.02.058_bib13 article-title: A reversible defect in natural killer T cell function characterizes the progression of premalignant to malignant multiple myeloma publication-title: J. Exp. Med. doi: 10.1084/jem.20021650 – volume: 166 start-page: 6578 year: 2001 ident: 10.1016/j.celrep.2018.02.058_bib36 article-title: Mechanisms of the antimetastatic effect in the liver and of the hepatocyte injury induced by alpha-galactosylceramide in mice publication-title: J. Immunol. doi: 10.4049/jimmunol.166.11.6578 – volume: 5 start-page: e11311 year: 2010 ident: 10.1016/j.celrep.2018.02.058_bib38 article-title: Defective NKT cell activation by CD1d+ TRAMP prostate tumor cells is corrected by interleukin-12 with α-galactosylceramide publication-title: PLoS ONE doi: 10.1371/journal.pone.0011311 – volume: 30 start-page: 567 year: 2012 ident: 10.1016/j.celrep.2018.02.058_bib43 article-title: Circulating invariant natural killer T-cell numbers predict outcome in head and neck squamous cell carcinoma: updated analysis with 10-year follow-up publication-title: J. Clin. Oncol. doi: 10.1200/JCO.2011.38.8819 – volume: 11 start-page: 1039 year: 2010 ident: 10.1016/j.celrep.2018.02.058_bib12 article-title: Invariant NKT cells modulate the suppressive activity of IL-10-secreting neutrophils differentiated with serum amyloid A publication-title: Nat. Immunol. doi: 10.1038/ni.1942 – volume: 23 start-page: 3510 year: 2017 ident: 10.1016/j.celrep.2018.02.058_bib14 article-title: Adoptive transfer of invariant NKT cells as immunotherapy for advanced melanoma: a phase I clinical trial publication-title: Clin. Cancer Res. doi: 10.1158/1078-0432.CCR-16-0600 |
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| SubjectTerms | angiogenesis Animals CD1d CD40 CD40 Antigens - metabolism Disease Progression Fas Humans immunotherapy iNKT cells macrophage Macrophages - metabolism Male Mice Natural Killer T-Cells - immunology prostate cancer Prostatic Neoplasms - genetics Prostatic Neoplasms - metabolism Prostatic Neoplasms - pathology tumor microenvironment |
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| Title | Bimodal CD40/Fas-Dependent Crosstalk between iNKT Cells and Tumor-Associated Macrophages Impairs Prostate Cancer Progression |
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