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1. Nucleotide metabolism in cancer cells fuels a UDP-driven macrophage cross-talk, promoting immunosuppression and immunotherapy resistance

Author

Scolaro, Tommaso, Manco, Marta, Pecqueux, Mathieu, Amorim, Ricardo, Trotta, Rosa, Van Acker, Heleen H., Van Haele, Matthias, Shirgaonkar, Niranjan, Naulaerts, Stefan, Daniluk, Jan, Prenen, Fran, Varamo, Chiara, Ponti, Donatella, Doglioni, Ginevra, Ferreira Campos, Ana Margarida, Fernandez Garcia, Juan, Radenkovic, Silvia, Rouhi, Pegah, Beatovic, Aleksandar, Wang, Liwei, Wang, Yu, Tzoumpa, Amalia, Antoranz, Asier, Sargsian, Ara, Di Matteo, Mario, Berardi, Emanuele, Goveia, Jermaine, Ghesquière, Bart, Roskams, Tania, Soenen, Stefaan, Voets, Thomas, Manshian, Bella, Fendt, Sarah-Maria, Carmeliet, Peter, Garg, Abhishek D., DasGupta, Ramanuj, Topal, Baki, and Mazzone, Massimiliano

Published
2024
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5. Supplementary Data from Plexin-A4 Mediates Cytotoxic T-cell Trafficking and Exclusion in Cancer

Author

Celus, Ward, primary, Oliveira, Ana I., primary, Rivis, Silvia, primary, Van Acker, Heleen H., primary, Landeloos, Ewout, primary, Serneels, Jens, primary, Cafarello, Sarah Trusso, primary, Van Herck, Yannick, primary, Mastrantonio, Roberta, primary, Köhler, Arnaud, primary, Garg, Abhishek D., primary, Flamand, Véronique, primary, Tamagnone, Luca, primary, Marine, Jean-Christophe, primary, Matteo, Mario Di, primary, Costa, Bruno M., primary, Bechter, Oliver, primary, and Mazzone, Massimiliano, primary

Published
2023
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6. Data from Plexin-A4 Mediates Cytotoxic T-cell Trafficking and Exclusion in Cancer

Author

Celus, Ward, primary, Oliveira, Ana I., primary, Rivis, Silvia, primary, Van Acker, Heleen H., primary, Landeloos, Ewout, primary, Serneels, Jens, primary, Cafarello, Sarah Trusso, primary, Van Herck, Yannick, primary, Mastrantonio, Roberta, primary, Köhler, Arnaud, primary, Garg, Abhishek D., primary, Flamand, Véronique, primary, Tamagnone, Luca, primary, Marine, Jean-Christophe, primary, Matteo, Mario Di, primary, Costa, Bruno M., primary, Bechter, Oliver, primary, and Mazzone, Massimiliano, primary

Published
2023
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9. Plexin-A4 Mediates Cytotoxic T-cell Trafficking and Exclusion in Cancer

Author

Celus, Ward, Oliveira, Ana A.I., Rivis, Silvia, Van Acker, Heleen, Landeloos, Ewout, Serneels, Jens, Cafarello, Sarah Trusso, Van Herck, Yannick, Mastrantonio, Roberta, Kohler, Arnaud, Garg, Abhishek A.D., Flamand, Véronique, Tamagnone, Luca, Marine, Jean-Christophe, Di Matteo, Mario, Costa, Bruno, Bechter, Oliver, Mazzone, Massimiliano, Celus, Ward, Oliveira, Ana A.I., Rivis, Silvia, Van Acker, Heleen, Landeloos, Ewout, Serneels, Jens, Cafarello, Sarah Trusso, Van Herck, Yannick, Mastrantonio, Roberta, Kohler, Arnaud, Garg, Abhishek A.D., Flamand, Véronique, Tamagnone, Luca, Marine, Jean-Christophe, Di Matteo, Mario, Costa, Bruno, Bechter, Oliver, and Mazzone, Massimiliano

Abstract

Cytotoxic T cell (CTL) infiltration of the tumor carries the potential to limit cancer progression, but their exclusion by the immunosuppressive tumor microenvironment hampers the efficiency of immunotherapy. Here, we show that expression of the axon guidance molecule Plexin-A4 (Plxna4) in CTLs, especially in effector/memory CD8 T cells, is induced upon T-cell activation, sustained in the circulation, but reduced when entering the tumor bed. Therefore, we deleted Plxna4 and observed that Plxna4-deficient CTLs acquired improved homing capacity to the lymph nodes and to the tumor, as well as increased proliferation, both achieved through enhanced Rac1 activation. Mice with stromal or hematopoietic Plxna4 deletion exhibited enhanced CTL infiltration and impaired tumor growth. In a melanoma model, adoptive transfer of CTLs lacking Plxna4 prolonged survival and improved therapeutic outcome, which was even stronger when combined with anti-programmed cell death protein 1 (PD-1) treatment. PLXNA4 abundance in circulating CTLs was augmented in melanoma patients versus healthy volunteers but decreased after the first cycle of anti-PD-1, alone or in combination with anti-cytotoxic T-Lymphocyte Associated Protein 4 (CTLA-4), in those patients showing complete or partial response to the treatment. Altogether, our data suggest that Plxna4 acts as a "checkpoint," negatively regulating CTL migration and proliferation through cell-autonomous mechanisms independent of the interaction with host-derived Plxna4 ligands, semaphorins. These findings pave the way toward Plxna4-centric immunotherapies and propose Plxna4 detection in circulating CTLs as a potential way to monitor the response to immune checkpoint blockade in patients with metastatic melanoma., SCOPUS: ar.j, info:eu-repo/semantics/published

Published
2022

10. Engineering monocyte-derived dendritic cells to secrete interferon-α enhances their ability to promote adaptive and innate anti-tumor immune effector functions

Author

Willemen, Yannick, Van den Bergh, Johan M. J., Lion, Eva, Anguille, Sébastien, Roelandts, Vicky A. E., Van Acker, Heleen H., Heynderickx, Steven D. I., Stein, Barbara M. H., Peeters, Marc, Figdor, Carl G., Van Tendeloo, Viggo F. I., de Vries, I. Jolanda, Adema, Gosse J., Berneman, Zwi N., and Smits, Evelien L. J.

Published
2015
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12. Plexin-A4 Mediates Cytotoxic T-cell Trafficking and Exclusion in Cancer : PlexinA4 reguleert cytotoxische T-cel migratie en proliferatie bij kanker

Author

Celus, Ward, Oliveira, Ana, Rivis, Silvia, Van Acker, Heleen H, Landeloos, Ewout, Serneels, Jens, Cafarello, Sarah Trusso, Van Herck, Yannick, Mastrantonio, Roberta, Koehler, Arnaud, Garg, Abhishek D, Flamand, Veronique, Tamagnone, Luca, Marine, Jean-Christophe, Di Matteo, Mario, Costa, Bruno M, Bechter, Oliver, Mazzone, Massimiliano, Prenen, Hans, and Mazzone, Massimiliano

Abstract

Cytotoxic T cell (CTL) infiltration of the tumor carries the potential to limit cancer progression, but their exclusion by the immunosuppressive tumor microenvironment hampers the efficiency of immunotherapy. Here, we show that expression of the axon guidance molecule Plexin-A4 (Plxna4) in CTLs, especially in effector/memory CD8+ T cells, is induced upon T-cell activation, sustained in the circulation, but reduced when entering the tumor bed. Therefore, we deleted Plxna4 and observed that Plxna4-deficient CTLs acquired improved homing capacity to the lymph nodes and to the tumor, as well as increased proliferation, both achieved through enhanced Rac1 activation. Mice with stromal or hematopoietic Plxna4 deletion exhibited enhanced CTL infiltration and impaired tumor growth. In a melanoma model, adoptive transfer of CTLs lacking Plxna4 prolonged survival and improved therapeutic outcome, which was even stronger when combined with anti-programmed cell death protein 1 (PD-1) treatment. PLXNA4 abundance in circulating CTLs was augmented in melanoma patients versus healthy volunteers but decreased after the first cycle of anti-PD-1, alone or in combination with anti-cytotoxic T-Lymphocyte Associated Protein 4 (CTLA-4), in those patients showing complete or partial response to the treatment. Altogether, our data suggest that Plxna4 acts as a "checkpoint," negatively regulating CTL migration and proliferation through cell-autonomous mechanisms independent of the interaction with host-derived Plxna4 ligands, semaphorins. These findings pave the way toward Plxna4-centric immunotherapies and propose Plxna4 detection in circulating CTLs as a potential way to monitor the response to immune checkpoint blockade in patients with metastatic melanoma. ispartof: CANCER IMMUNOLOGY RESEARCH vol:10 issue:1 pages:126-141 ispartof: location:United States nrpages: 16 status: published

Published
2022

13. Plexin-A4 Mediates Cytotoxic T-cell Trafficking and Exclusion in Cancer

Author

Celus, Ward, primary, Oliveira, Ana I., additional, Rivis, Silvia, additional, Van Acker, Heleen H., additional, Landeloos, Ewout, additional, Serneels, Jens, additional, Cafarello, Sarah Trusso, additional, Van Herck, Yannick, additional, Mastrantonio, Roberta, additional, Köhler, Arnaud, additional, Garg, Abhishek D., additional, Flamand, Véronique, additional, Tamagnone, Luca, additional, Marine, Jean-Christophe, additional, Matteo, Mario Di, additional, Costa, Bruno M., additional, Bechter, Oliver, additional, and Mazzone, Massimiliano, additional

Published
2021
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15. Rothia mucilaginosa is an anti-inflammatory bacterium in the respiratory tract of patients with chronic lung disease

Author

Rigauts, Charlotte, primary, Aizawa, Juliana, additional, Taylor, Steven L., additional, Rogers, Geraint B., additional, Govaerts, Matthias, additional, Cos, Paul, additional, Ostyn, Lisa, additional, Sims, Sarah, additional, Vandeplassche, Eva, additional, Sze, Mozes, additional, Dondelinger, Yves, additional, Vereecke, Lars, additional, Van Acker, Heleen, additional, Simpson, Jodie L., additional, Burr, Lucy, additional, Willems, Anne, additional, Tunney, Michael M., additional, Cigana, Cristina, additional, Bragonzi, Alessandra, additional, Coenye, Tom, additional, and Crabbé, Aurélie, additional

Published
2021
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16. The commensal bacterium Rothia mucilaginosa has anti-inflammatory properties in vitro and in vivo, and negatively correlates with sputum pro-inflammatory markers in chronic airway disease

Author

Rigauts, Charlotte, primary, Aizawa, Juliana, additional, Taylor, Steven, additional, Rogers, Geraint, additional, Govaerts, Matthias, additional, Cos, Paul, additional, Ostyn, Lisa, additional, Sims, Sarah, additional, Vandeplassche, Eva, additional, Sze, Mozes, additional, Dondelinger, Yves, additional, Vereecke, Lars, additional, Van Acker, Heleen, additional, Simpson, Jodie, additional, Burr, Lucy, additional, Willems, Anne, additional, Tunney, Michael, additional, Cigana, Cristina, additional, Bragonzi, Alessandra, additional, Coenye, Tom, additional, and Crabbé, Aurélie, additional

Published
2021
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17. PlexinA4 mediates cytotoxic T cell trafficking and exclusion in cancer

Author

Celus, Ward, I Oliveira, Ana, Rivis, Silvia, H Van Acker, Heleen, Landeloos, Ewout, Serneels, Jen, Trusso Cafarello, Sarah, Van Herck, Yannick, Mastrantonio, Roberta, Köhler, Arnaud, D Garg, Abhishek, Flamand, Véronique, Tamagnone, Luca, Marine, Jean-Christophe, Di Matteo, Mario, M Costa, Bruno, Bechter, Oliver, Mazzone, Massimiliano, Roberta Mastrantonio (ORCID:0000-0002-1764-457X), Luca Tamagnone (ORCID:0000-0002-2884-7946), Celus, Ward, I Oliveira, Ana, Rivis, Silvia, H Van Acker, Heleen, Landeloos, Ewout, Serneels, Jen, Trusso Cafarello, Sarah, Van Herck, Yannick, Mastrantonio, Roberta, Köhler, Arnaud, D Garg, Abhishek, Flamand, Véronique, Tamagnone, Luca, Marine, Jean-Christophe, Di Matteo, Mario, M Costa, Bruno, Bechter, Oliver, Mazzone, Massimiliano, Roberta Mastrantonio (ORCID:0000-0002-1764-457X), and Luca Tamagnone (ORCID:0000-0002-2884-7946)

Abstract

Cytotoxic T cell (CTL) infiltration of the tumor carries the potential to limit cancer progression, but their exclusion by the immunosuppressive tumor microenvironment hampers the efficiency of immunotherapy. Here, we show that expression of the axon guidance molecule PlexinA4 (Plxna4) in CTLs, especially in effector/memory CD8+ T cells, is induced upon T-cell activation, sustained in the circulation, but reduced when entering the tumor bed. Therefore, we deleted Plxna4 and observed that Plxna4-deficient CTLs acquired improved homing capacity to the lymph nodes and to the tumor, as well as increased proliferation, both achieved through enhanced Rac1 activation. Mice with stromal or hematopoietic Plxna4 deletion exhibited enhanced CTL infiltration and impaired tumor growth. In a melanoma model, adoptive transfer of CTLs lacking Plxna4 prolonged survival and improved therapeutic outcome, which was even stronger when combined with anti-PD-1 treatment. PLXNA4 abundance in circulating CTLs was augmented in melanoma patients versus healthy volunteers but decreased after the first cycle of anti-PD-1, alone or in combination with anti-CTLA-4, in those patients showing complete or partial response to the treatment. Altogether, our data suggest that PlexinA4 acts as a "checkpoint", negatively regulating CTL migration and proliferation through cell autonomous mechanisms independent of the interaction with host-derived PlexinA4 ligands semaphorins. These findings pave the way towards PlexinA4-centric immunotherapies and propose PlexinA4 detection in circulating CTLs as a potential way to monitor the response to immune checkpoint blockade in metastatic melanoma patients.

Published
2021

22. The role of small proteins in Burkholderia cenocepacia J2315 biofilm formation, persistence and intracellular growth

Author

Van Acker, Heleen, primary, Crabbé, Aurélie, additional, Jurėnas, Dukas, additional, Ostyn, Lisa, additional, Sass, Andrea, additional, Daled, Simon, additional, Dhaenens, Maarten, additional, Deforce, Dieter, additional, Teirlinck, Eline, additional, De Keersmaecker, Herlinde, additional, Braeckmans, Kevin, additional, Van Melderen, Laurence, additional, and Coenye, Tom, additional

Published
2019
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23. The role of small proteins in Burkholderia cenocepacia J2315 biofilm formation, persistence and intracellular growth

Author

Van Acker, Heleen, Crabbé, Aurélie, Jurenas, Dukas, Ostyn, Lisa, Sass, Andrea, Daled, Simon, Dhaenens, Maarten, Deforce, Dieter, Teirlinck, Eline, De Keersmaecker, Herlinde, Braeckmans, Kevin, Van Melderen, Laurence, Coenye, Tom, Van Acker, Heleen, Crabbé, Aurélie, Jurenas, Dukas, Ostyn, Lisa, Sass, Andrea, Daled, Simon, Dhaenens, Maarten, Deforce, Dieter, Teirlinck, Eline, De Keersmaecker, Herlinde, Braeckmans, Kevin, Van Melderen, Laurence, and Coenye, Tom

Abstract

Burkholderia cenocepacia infections are difficult to treat due to resistance, biofilm formation and persistence. B. cenocepacia strain J2315 has a large multi-replicon genome (8.06 Mb) and the function of a large fraction of (conserved) hypothetical genes remains elusive. The goal of the present study is to elucidate the role of small proteins in B. cenocepacia, focusing on genes smaller than 300 base pairs of which the function is unknown. Almost 10% (572) of the B. cenocepacia J2315 genes are smaller than 300 base pairs and more than half of these are annotated as coding for hypothetical proteins. For 234 of them no similarity could be found with non-hypothetical genes in other bacteria using BLAST. Using available RNA sequencing data obtained from biofilms, a list of 27 highly expressed B. cenocepacia J2315 genes coding for small proteins was compiled. For nine of them expression in biofilms was also confirmed using LC-MS based proteomics and/or expression was confirmed using eGFP translational fusions. Overexpression of two of these genes negatively impacted growth, whereas for four others overexpression led to an increase in biofilm biomass. Overexpression did not have an influence on the MIC for tobramycin, ciprofloxacin or meropenem but for five small protein encoding genes, overexpression had an effect on the number of persister cells in biofilms. While there were no significant differences in adherence to and invasion of A549 epithelial cells between the overexpression mutants and the WT, significant differences were observed in intracellular growth/survival. Finally, the small protein BCAM0271 was identified as an antitoxin belonging to a toxin-antitoxin module. The toxin was found to encode a tRNA acetylase that inhibits translation. In conclusion, our results confirm that small proteins are present in the genome of B. cenocepacia J2315 and indicate that they are involved in various biological processes, including biofilm formation, persistence and intrac, SCOPUS: ar.j, info:eu-repo/semantics/published

Published
2019

28. Dendritic Cell-Based Immunotherapy of Acute Myeloid Leukemia

Author

Van Acker, Heleen H., primary, Versteven, Maarten, additional, Lichtenegger, Felix S., additional, Roex, Gils, additional, Campillo-Davo, Diana, additional, Lion, Eva, additional, Subklewe, Marion, additional, Van Tendeloo, Viggo F., additional, Berneman, Zwi N., additional, and Anguille, Sébastien, additional

Published
2019
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29. Various Evolutionary Trajectories Lead to Loss of the Tobramycin-Potentiating Activity of the Quorum-Sensing Inhibitor Baicalin Hydrate in Burkholderia cenocepacia Biofilms

Author

Sass, Andrea, primary, Slachmuylders, Lisa, additional, Van Acker, Heleen, additional, Vandenbussche, Ian, additional, Ostyn, Lisa, additional, Bové, Mona, additional, Crabbé, Aurélie, additional, Chiarelli, Laurent R., additional, Buroni, Silvia, additional, Van Nieuwerburgh, Filip, additional, Abatih, Emmanuel, additional, and Coenye, Tom, additional

Published
2019
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35. Chimeric Antigen Receptor-Engineered Human Gamma Delta T Cells: Enhanced Cytotoxicity with Retention of Cross Presentation

Author

Capsomidis, Anna, primary, Benthall, Gabriel, additional, Van Acker, Heleen H., additional, Fisher, Jonathan, additional, Kramer, Anne M., additional, Abeln, Zarah, additional, Majani, Yvonne, additional, Gileadi, Talia, additional, Wallace, Rebecca, additional, Gustafsson, Kenth, additional, Flutter, Barry, additional, and Anderson, John, additional

Published
2018
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38. Desirable cytolytic immune effector cell recruitment by interleukin-15 dendritic cells

Author

Van Acker, Heleen H., primary, Beretta, Ottavio, additional, Anguille, Sébastien, additional, Caluwé, Lien De, additional, Papagna, Angela, additional, Van den Bergh, Johan M., additional, Willemen, Yannick, additional, Goossens, Herman, additional, Berneman, Zwi N., additional, Van Tendeloo, Viggo F., additional, Smits, Evelien L., additional, Foti, Maria, additional, and Lion, Eva, additional

Published
2017
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40. Molecular mechanisms of persistence in Burkholderia cenocepacia biofilms

Author

Van Acker, Heleen, Coenye, Tom, and Nelis, Hans

Subjects
Burkholderia, Biology and Life Sciences, ROS, persistence, biochemical phenomena, metabolism, and nutrition, toxin antitoxin modules, biofilm
Abstract

Burkholderia cenocepacia J2315 is a member of the Burkholderia cepacia complex (Bcc), a group of 18 closely related metabolically versatile microorganisms. These opportunistic pathogens can cause severe lung infections in cystic fibrosis patients. Infections are often difficult to treat due to innate resistance of Bcc species to antimicrobials and because of their capacity to form biofilms. One of the mechanisms thought to be involved in biofilm resilience is the presence of persister cells. The main aim of this dissertation was to investigate whether persister cells are present in B. cenocepacia biofilms, what the molecular basis of antimicrobial tolerance is, and how persisters can be eradicated. We confirmed the presence of persister cells in B. cenocepacia biofilms and found that genes encoding proteins involved in ROS production are downregulated in persister cells, whereas the glyoxylate shunt is upregulated. Additionally, we found that toxin antitoxin (TA)-modules are involved in persistence. Searching for TA-modules we also identified an interesting operon (BCAM0257-8) located in the B. cepacia epidemic strain marker region. This module plays a role in persistence and in addition, BCAM0258 functions as a regulator influencing quorum sensing and activating cellular pathways involved in iron acquisition and biofilm formation. Overexpression of BCAM0257 was found to increase virulence in Galleria mellonella. Genes similar to BCAM0257-8 are found in all sequenced B. cenocepacia ET-12 genomes and its presence may help explaining why infections with strains of the B. cenocepacia ET-12 lineage are so difficult to treat. Furthermore, we evaluated in vitro the bacteriostatic and bactericidal activity of temocillin, a 6-α-methoxy-penicillin against planktonic and sessile Bcc bacteria. Our data indicate that, although temocillin has a good bacteriostatic activity against planktonic cultures and 4-h old biofilms, it is of limited use to eradicate mature biofilms.

Published
2014

47. Dendritic Cells as Pharmacological Tools for Cancer Immunotherapy

Author

Anguille, Sébastien, primary, Smits, Evelien L., additional, Bryant, Christian, additional, Van Acker, Heleen H., additional, Goossens, Herman, additional, Lion, Eva, additional, Fromm, Phillip D., additional, Hart, Derek N., additional, Van Tendeloo, Viggo F., additional, and Berneman, Zwi N., additional

Published
2015
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