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2. Author Correction: Tumor immunoevasion by the conversion of effector NK cells into type 1 innate lymphoid cell

Author

Gao, Yulong, Souza-Fonseca-Guimaraes, Fernando, Bald, Tobias, Ng, Susanna S., Young, Arabella, Ngiow, Shin Foong, Rautela, Jai, Straube, Jasmin, Waddell, Nic, Blake, Stephen J., Yan, Juming, Bartholin, Laurent, Lee, Jason S., Vivier, Eric, Takeda, Kazuyoshi, Messaoudene, Meriem, Zitvogel, Laurence, Teng, Michele W. L., Belz, Gabrielle T., Engwerda, Christian R., Huntington, Nicholas D., Nakamura, Kyohei, Hölzel, Michael, and Smyth, Mark J.

Published
2024
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3. Retraction: NK cell heparanase controls tumor invasion and immune surveillance

Author

Putz, Eva M., Mayfosh, Alyce J., Kos, Kevin, Barkauskas, Deborah S., Nakamura, Kyohei, Town, Liam, Goodall, Katharine J., Yee, Dean Y., Poon, Ivan K.H., Baschuk, Nikola, Souza-Fonseca-Guimaraes, Fernando, Hulett, Mark D., and Smyth, Mark J.

Subjects
Health care industry
Abstract

Original citation: J Clin Invest. 2017;127(7):2777-2788. https://doi.org/10.1172/JCI92958. Citation for this retraction: J Clin Invest. 2024;134(13):e183295. https://doi.org/10.1172/JCI183295. QIMR Berghofer Medical Research Institute recently notified the JCI of concerns regarding Figure 3C [...]

Published
2024

4. Retraction: TIGIT predominantly regulates the immune response via regulatory T cells

Author

Kurtulus, Sema, Sakuishi, Kaori, Ngiow, Shin-Foong, Joller, Nicole, Tan, Dewar J., Teng, Michele W.L., Smyth, Mark J., Kuchroo, Vijay K., and Anderson, Ana C.

Subjects
Health care industry
Abstract

Original citation: J Clin Invest. 2015;125(11):4053-4062. https://doi.org/10.1172/JCI81187. Citation for this retraction: J Clin Invest. 2024;134(13):e183278. https://doi.org/10.1172/JCI183278. QIMR Berghofer Medical Research Institute recently notified the JCI of concerns regarding Figure 4B [...]

Published
2024

5. Author Correction: CIS is a potent checkpoint in NK cell–mediated tumor immunity

Author

Delconte, Rebecca B., Kolesnik, Tatiana B., Dagley, Laura F., Rautela, Jai, Shi, Wei, Putz, Eva M., Stannard, Kimberley, Zhang, Jian-Guo, Teh, Charis, Firth, Matt, Ushiki, Takashi, Andoniou, Christopher E., Degli-Esposti, Mariapia A., Sharp, Phillip P., Sanvitale, Caroline E., Infusini, Giuseppe, Liau, Nicholas P. D., Linossi, Edmond M., Burns, Christopher J., Carotta, Sebastian, Gray, Daniel H. D., Seillet, Cyril, Hutchinson, Dana S., Belz, Gabrielle T., Webb, Andrew I., Alexander, Warren S., Li, Shawn S., Bullock, Alex N., Babon, Jeffrey J., Smyth, Mark J., Nicholson, Sandra E., and Huntington, Nicholas D.

Published
2024
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6. Multiple functions of CXCL12 in a syngeneic model of breast cancer

Author

Smyth Mark J, Anderson Robin L, Comerford Iain, Harata-Lee Yuka, Williams Sharon A, and McColl Shaun R

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract Background A growing body of work implicates chemokines, in particular CXCL12 and its receptors, in the progression and site-specific metastasis of various cancers, including breast cancer. Various agents have been used to block the CXCL12-CXCR4 interaction as a means of inhibiting cancer metastasis. However, as a potent chemotactic factor for leukocytes, CXCL12 also has the potential to enhance anti-cancer immunity. To further elucidate its role in breast cancer progression, CXCL12 and its antagonist CXCL12(P2G) were overexpressed in the syngeneic 4T1.2 mouse model of breast carcinoma. Results While expression of CXCL12(P2G) significantly inhibited metastasis, expression of wild-type CXCL12 potently inhibited both metastasis and primary tumor growth. The effects of wild-type CXCL12 were attributed to an immune response characterized by the induction of CD8+ T cell activity, enhanced cell-mediated cytotoxicity, increased numbers of CD11c+ cells in the tumor-draining lymph nodes and reduced accumulation of myeloid-derived suppressor cells in the spleen. Conclusions This study highlights the need to consider carefully therapeutic strategies that block CXCL12 signaling. Therapies that boost CXCL12 levels at the primary tumor site may prove more effective in the treatment of metastatic breast cancer.

Published
2010
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7. Three agonist antibodies in combination with high-dose IL-2 eradicate orthotopic kidney cancer in mice

Author

Sharkey Janelle, Guru Preethi, Darcy Phillip K, Westwood Jennifer A, Pegram Hollie J, Amos Sally M, Smyth Mark J, and Kershaw Michael H

Subjects
Medicine
Abstract

Abstract Background Combination immunotherapies can be effective against subcutaneous tumors in mice but the effect against orthotopic malignant disease is less well characterized. In particular, a combination of three agonist antibodies, termed Tri-mAb, consisting of anti-DR5, anti-CD40 and anti-CD137 has previously been demonstrated to eradicate a large proportion of subcutaneous renal cell carcinoma (Renca) tumors (75% long-term survival), but the effect against orthotopic disease is not known. Purpose To determine the relative response of orthotopic tumors, we inoculated Renca into the kidney followed by treatment with Tri-mAb. Results We found that orthotopic tumors responded much less to treatment (~13% survival), but a significant improvement in survival was achieved through the addition of IL-2 to the treatment regimen (55% survival). All three agonist antibodies and high dose IL-2, 100,000 IU for up to six doses, were required. CD8+ T cells were also required for optimal anti-tumor responses. Coadministration of IL-2 led to enhanced T cell activity as demonstrated by an increased frequency of IFN-gamma-producing T cells in tumor-draining lymph nodes, which may have contributed to the observed improvement of therapy against kidney tumors. Implications Responses of subcutaneous tumors to immunotherapy do not necessarily reflect how orthotopic tumors respond. The use of combination immunotherapy stimulating multiple facets of immunity and including cytokine support for T cells can induce effective anti-tumor responses against orthotopic and metastatic tumors.

Published
2010
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8. Author Correction: The NK cell granule protein NKG7 regulates cytotoxic granule exocytosis and inflammation

Author

Ng, Susanna S., De Labastida Rivera, Fabian, Yan, Juming, Corvino, Dillon, Das, Indrajit, Zhang, Ping, Kuns, Rachel, Chauhan, Shashi Bhushan, Hou, Jiajie, Li, Xian-Yang, Frame, Teija C. M., McEnroe, Benjamin A., Moore, Eilish, Na, Jinrui, Engel, Jessica A., Soon, Megan S. F., Singh, Bhawana, Kueh, Andrew J., Herold, Marco J., Montes de Oca, Marcela, Singh, Siddharth Sankar, Bunn, Patrick T., Aguilera, Amy Roman, Casey, Mika, Braun, Matthias, Ghazanfari, Nazanin, Wani, Shivangi, Wang, Yulin, Amante, Fiona H., Edwards, Chelsea L., Haque, Ashraful, Dougall, William C., Singh, Om Prakash, Baxter, Alan G., Teng, Michele W. L., Loukas, Alex, Daly, Norelle L., Cloonan, Nicole, Degli-Esposti, Mariapia A., Uzonna, Jude, Heath, William R., Bald, Tobias, Tey, Siok-Keen, Nakamura, Kyohei, Hill, Geoffrey R., Kumar, Rajiv, Sundar, Shyam, Smyth, Mark J., and Engwerda, Christian R.

Published
2024
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9. The NK cell–cancer cycle: advances and new challenges in NK cell–based immunotherapies

Author

Bald, Tobias, Krummel, Matthew F, Smyth, Mark J, and Barry, Kevin C

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Immunology, Cancer, Immunization, Immunotherapy, Biotechnology, 2.1 Biological and endogenous factors, 5.2 Cellular and gene therapies, Animals, Humans, Killer Cells, Natural, Neoplasms, Tumor Microenvironment, Biochemistry and cell biology
Abstract

Natural killer (NK) cells belong to the innate immune system and contribute to protecting the host through killing of infected, foreign, stressed or transformed cells. Additionally, via cellular cross-talk, NK cells orchestrate antitumor immune responses. Hence, significant efforts have been undertaken to exploit the therapeutic properties of NK cells in cancer. Current strategies in preclinical and clinical development include adoptive transfer therapies, direct stimulation, recruitment of NK cells into the tumor microenvironment (TME), blockade of inhibitory receptors that limit NK cell functions, and therapeutic modulation of the TME to enhance antitumor NK cell function. In this Review, we introduce the NK cell-cancer cycle to highlight recent advances in NK cell biology and to discuss the progress and problems of NK cell-based cancer immunotherapies.

Published
2020

10. Consensus guidelines for the definition, detection and interpretation of immunogenic cell death

Author

Galluzzi, Lorenzo, Vitale, Ilio, Warren, Sarah, Adjemian, Sandy, Agostinis, Patrizia, Martinez, Aitziber Buqué, Chan, Timothy A, Coukos, George, Demaria, Sandra, Deutsch, Eric, Draganov, Dobrin, Edelson, Richard L, Formenti, Silvia C, Fucikova, Jitka, Gabriele, Lucia, Gaipl, Udo S, Gameiro, Sofia R, Garg, Abhishek D, Golden, Encouse, Han, Jian, Harrington, Kevin J, Hemminki, Akseli, Hodge, James W, Hossain, Dewan Md Sakib, Illidge, Tim, Karin, Michael, Kaufman, Howard L, Kepp, Oliver, Kroemer, Guido, Lasarte, Juan Jose, Loi, Sherene, Lotze, Michael T, Manic, Gwenola, Merghoub, Taha, Melcher, Alan A, Mossman, Karen L, Prosper, Felipe, Rekdal, Øystein, Rescigno, Maria, Riganti, Chiara, Sistigu, Antonella, Smyth, Mark J, Spisek, Radek, Stagg, John, Strauss, Bryan E, Tang, Daolin, Tatsuno, Kazuki, van Gool, Stefaan W, Vandenabeele, Peter, Yamazaki, Takahiro, Zamarin, Dmitriy, Zitvogel, Laurence, Cesano, Alessandra, and Marincola, Francesco M

Subjects
Inflammatory and immune system, Consensus, Guidelines as Topic, Humans, Immunogenic Cell Death, Molecular Biology, oncology, immunology, molecular biology
Abstract

Cells succumbing to stress via regulated cell death (RCD) can initiate an adaptive immune response associated with immunological memory, provided they display sufficient antigenicity and adjuvanticity. Moreover, multiple intracellular and microenvironmental features determine the propensity of RCD to drive adaptive immunity. Here, we provide an updated operational definition of immunogenic cell death (ICD), discuss the key factors that dictate the ability of dying cells to drive an adaptive immune response, summarize experimental assays that are currently available for the assessment of ICD in vitro and in vivo, and formulate guidelines for their interpretation.

Published
2020

11. BET inhibition blocks inflammation-induced cardiac dysfunction and SARS-CoV-2 infection

Author

Mills, Richard J., Humphrey, Sean J., Fortuna, Patrick R.J., Lor, Mary, Foster, Simon R., Quaife-Ryan, Gregory A., Johnston, Rebecca L., Dumenil, Troy, Bishop, Cameron, Rudraraju, Rajeev, Rawle, Daniel J., Le, Thuy, Zhao, Wei, Lee, Leo, Mackenzie-Kludas, Charley, Mehdiabadi, Neda R., Halliday, Christopher, Gilham, Dean, Fu, Li, Nicholls, Stephen J., Johansson, Jan, Sweeney, Michael, Wong, Norman C.W., Kulikowski, Ewelina, Sokolowski, Kamil A., Tse, Brian W.C., Devilée, Lynn, Voges, Holly K., Reynolds, Liam T., Krumeich, Sophie, Mathieson, Ellen, Abu-Bonsrah, Dad, Karavendzas, Kathy, Griffen, Brendan, Titmarsh, Drew, Elliott, David A., McMahon, James, Suhrbier, Andreas, Subbarao, Kanta, Porrello, Enzo R., Smyth, Mark J., Engwerda, Christian R., MacDonald, Kelli P.A., Bald, Tobias, James, David E., and Hudson, James E.

Published
2021
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14. CD155 on Tumor Cells Drives Resistance to Immunotherapy by Inducing the Degradation of the Activating Receptor CD226 in CD8+ T Cells

Author

Braun, Matthias, Aguilera, Amelia Roman, Sundarrajan, Ashmitha, Corvino, Dillon, Stannard, Kimberley, Krumeich, Sophie, Das, Indrajit, Lima, Luize G., Meza Guzman, Lizeth G., Li, Kunlun, Li, Rui, Salim, Nazhifah, Jorge, Maria Villancanas, Ham, Sunyoung, Kelly, Gabrielle, Vari, Frank, Lepletier, Ailin, Raghavendra, Ashwini, Pearson, Sally, Madore, Jason, Jacquelin, Sebastien, Effern, Maike, Quine, Brodie, Koufariotis, Lambros T., Casey, Mika, Nakamura, Kyohei, Seo, Eun Y., Hölzel, Michael, Geyer, Matthias, Kristiansen, Glen, Taheri, Touraj, Ahern, Elizabeth, Hughes, Brett G.M., Wilmott, James S., Long, Georgina V., Scolyer, Richard A., Batstone, Martin D., Landsberg, Jennifer, Dietrich, Dimo, Pop, Oltin T., Flatz, Lukas, Dougall, William C., Veillette, André, Nicholson, Sandra E., Möller, Andreas, Johnston, Robert J., Martinet, Ludovic, Smyth, Mark J., and Bald, Tobias

Published
2020
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15. Eomes-Dependent Loss of the Co-activating Receptor CD226 Restrains CD8+ T Cell Anti-tumor Functions and Limits the Efficacy of Cancer Immunotherapy

Author

Weulersse, Marianne, Asrir, Assia, Pichler, Andrea C., Lemaitre, Lea, Braun, Matthias, Carrié, Nadège, Joubert, Marie-Véronique, Le Moine, Marie, Do Souto, Laura, Gaud, Guillaume, Das, Indrajit, Brauns, Elisa, Scarlata, Clara M., Morandi, Elena, Sundarrajan, Ashmitha, Cuisinier, Marine, Buisson, Laure, Maheo, Sabrina, Kassem, Sahar, Agesta, Arantxa, Pérès, Michaël, Verhoeyen, Els, Martinez, Alejandra, Mazieres, Julien, Dupré, Loïc, Gossye, Thomas, Pancaldi, Vera, Guillerey, Camille, Ayyoub, Maha, Dejean, Anne S., Saoudi, Abdelhadi, Goriely, Stanislas, Avet-Loiseau, Hervé, Bald, Tobias, Smyth, Mark J., and Martinet, Ludovic

Published
2020
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18. Type I Interferons Suppress Anti-parasitic Immunity and Can Be Targeted to Improve Treatment of Visceral Leishmaniasis

Author

Kumar, Rajiv, Bunn, Patrick T., Singh, Siddharth Sankar, Ng, Susanna S., Montes de Oca, Marcela, De Labastida Rivera, Fabian, Chauhan, Shashi Bhushan, Singh, Neetu, Faleiro, Rebecca J., Edwards, Chelsea L., Frame, Teija C.M., Sheel, Meru, Austin, Rebecca J., Lane, Steven W., Bald, Tobias, Smyth, Mark J., Hill, Geoffrey.R., Best, Shannon E., Haque, Ashraful, Corvino, Dillon, Waddell, Nic, Koufariotis, Lambross, Mukhopadhay, Pamela, Rai, Madhukar, Chakravarty, Jaya, Singh, Om Prakash, Sacks, David, Nylen, Susanne, Uzonna, Jude, Sundar, Shyam, and Engwerda, Christian R.

Published
2020
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22. The NK cell granule protein NKG7 regulates cytotoxic granule exocytosis and inflammation

Author

Ng, Susanna S., De Labastida Rivera, Fabian, Yan, Juming, Corvino, Dillon, Das, Indrajit, Zhang, Ping, Kuns, Rachel, Chauhan, Shashi Bhushan, Hou, Jiajie, Li, Xian-Yang, Frame, Teija C. M., McEnroe, Benjamin A., Moore, Eilish, Na, Jinrui, Engel, Jessica A., Soon, Megan S. F., Singh, Bhawana, Kueh, Andrew J., Herold, Marco J., Montes de Oca, Marcela, Singh, Siddharth Sankar, Bunn, Patrick T., Aguilera, Amy Roman, Casey, Mika, Braun, Matthias, Ghazanfari, Nazanin, Wani, Shivangi, Wang, Yulin, Amante, Fiona H., Edwards, Chelsea L., Haque, Ashraful, Dougall, William C., Singh, Om Prakash, Baxter, Alan G., Teng, Michele W. L., Loukas, Alex, Daly, Norelle L., Cloonan, Nicole, Degli-Esposti, Mariapia A., Uzonna, Jude, Heath, William R., Bald, Tobias, Tey, Siok-Keen, Nakamura, Kyohei, Hill, Geoffrey R., Kumar, Rajiv, Sundar, Shyam, Smyth, Mark J., and Engwerda, Christian R.

Published
2020
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24. Classifying Cancers Based on T-cell Infiltration and PD-L1

Author

Teng, Michele WL, Ngiow, Shin Foong, Ribas, Antoni, and Smyth, Mark J

Subjects
Lung, Immunization, Cancer, Vaccine Related, Lung Cancer, B7-H1 Antigen, CD8-Positive T-Lymphocytes, Gene Expression Regulation, Neoplastic, Humans, Immunotherapy, Lymphocytes, Tumor-Infiltrating, Neoplasms, Tumor Microenvironment, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

Cancer immunotherapy may become a major treatment backbone in many cancers over the next decade. There are numerous immune cell types found in cancers and many components of an immune reaction to cancer. Thus, the tumor has many strategies to evade an immune response. It has been proposed that four different types of tumor microenvironment exist based on the presence or absence of tumor-infiltrating lymphocytes and programmed death-ligand 1 (PD-L1) expression. We review this stratification and the latest in a series of results that shed light on new approaches for rationally designing ideal combination cancer therapies based on tumor immunology.

Published
2015

25. Consensus nomenclature for CD8+ T cell phenotypes in cancer

Author

Apetoh, Lionel, Smyth, Mark J, Drake, Charles G, Abastado, Jean-Pierre, Apte, Ron N, Ayyoub, Maha, Blay, Jean-Yves, Bonneville, Marc, Butterfield, Lisa H, Caignard, Anne, Castelli, Chiara, Cavallo, Federica, Celis, Esteban, Chen, Lieping, Colombo, Mario P, Comin-Anduix, Begoña, Coukos, Georges, Dhodapkar, Madhav V, Dranoff, Glenn, Frazer, Ian H, Fridman, Wolf-Hervé, Gabrilovich, Dmitry I, Gilboa, Eli, Gnjatic, Sacha, Jäger, Dirk, Kalinski, Pawel, Kaufman, Howard L, Kiessling, Rolf, Kirkwood, John, Knuth, Alexander, Liblau, Roland, Lotze, Michael T, Lugli, Enrico, Marincola, Francesco, Melero, Ignacio, Melief, Cornelis J, Mempel, Thorsten R, Mittendorf, Elizabeth A, Odun, Kunle, Overwijk, Willem W, Palucka, Anna Karolina, Parmiani, Giorgio, Ribas, Antoni, Romero, Pedro, Schreiber, Robert D, Schuler, Gerold, Srivastava, Pramod K, Tartour, Eric, Valmori, Danila, van der Burg, Sjoerd H, van der Bruggen, Pierre, van den Eynde, Benoît J, Wang, Ena, Zou, Weiping, Whiteside, Theresa L, Speiser, Daniel E, Pardoll, Drew M, Restifo, Nicholas P, and Anderson, Ana C

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Immunology, Cancer, 2.1 Biological and endogenous factors, Aetiology, anergy, anticancer immunity, CD8(+) T cells, cytotoxicity, exhaustion, effector, IFN gamma, senescence, stemness, CD8+ T cells, IFNγ, Oncology and carcinogenesis
Abstract

Whereas preclinical investigations and clinical studies have established that CD8+ T cells can profoundly affect cancer progression, the underlying mechanisms are still elusive. Challenging the prevalent view that the beneficial effect of CD8+ T cells in cancer is solely attributable to their cytotoxic activity, several reports have indicated that the ability of CD8+ T cells to promote tumor regression is dependent on their cytokine secretion profile and their ability to self-renew. Evidence has also shown that the tumor microenvironment can disarm CD8+ T cell immunity, leading to the emergence of dysfunctional CD8+ T cells. The existence of different types of CD8+ T cells in cancer calls for a more precise definition of the CD8+ T cell immune phenotypes in cancer and the abandonment of the generic terms "pro-tumor" and "antitumor." Based on recent studies investigating the functions of CD8+ T cells in cancer, we here propose some guidelines to precisely define the functional states of CD8+ T cells in cancer.

Published
2015

26. Anticancer immunotherapy by CTLA-4 blockade: obligatory contribution of IL-2 receptors and negative prognostic impact of soluble CD25

Author

Hannani, Dalil, Vétizou, Marie, Enot, David, Rusakiewicz, Sylvie, Chaput, Nathalie, Klatzmann, David, Desbois, Melanie, Jacquelot, Nicolas, Vimond, Nadège, Chouaib, Salem, Mateus, Christine, Allison, James P, Ribas, Antoni, Wolchok, Jedd D, Yuan, Jianda, Wong, Philip, Postow, Michael, Mackiewicz, Andrzej, Mackiewicz, Jacek, Schadendorff, Dirk, Jaeger, Dirk, Korman, Alan J, Bahjat, Keith, Maio, Michele, Calabro, Luana, Teng, Michele WL, Smyth, Mark J, Eggermont, Alexander, Robert, Caroline, Kroemer, Guido, and Zitvogel, Laurence

Subjects
Cancer, Development of treatments and therapeutic interventions, 5.1 Pharmaceuticals, Adolescent, Adult, Aged, Aged, 80 and over, Animals, Antibodies, Monoclonal, CD4-Positive T-Lymphocytes, CTLA-4 Antigen, Cohort Studies, Disease Models, Animal, Female, Humans, Immunotherapy, Interleukin-2 Receptor alpha Subunit, Ipilimumab, Male, Melanoma, Mice, Mice, Inbred C57BL, Middle Aged, Receptors, Interleukin-2, Recombinant Proteins, T-Lymphocytes, Regulatory, Up-Regulation, Young Adult, ipilimumab, CTLA-4 blockade, IL-2, CD122, sCD25, tumor immunotherapy, cancer, Biochemistry and Cell Biology, Clinical Sciences, Developmental Biology
Abstract

The cytotoxic T lymphocyte antigen-4 (CTLA-4)-blocking antibody ipilimumab induces immune-mediated long-term control of metastatic melanoma in a fraction of patients. Although ipilimumab undoubtedly exerts its therapeutic effects via immunostimulation, thus far clinically useful, immunologically relevant biomarkers that predict treatment efficiency have been elusive. Here, we show that neutralization of IL-2 or blocking the α and β subunits of the IL-2 receptor (CD25 and CD122, respectively) abolished the antitumor effects and the accompanying improvement of the ratio of intratumoral T effector versus regulatory cells (Tregs), which were otherwise induced by CTLA-4 blockade in preclinical mouse models. CTLA-4 blockade led to the reduction of a suppressive CD4(+) T cell subset expressing Lag3, ICOS, IL-10 and Egr2 with a concomitant rise in IL-2-producing effector cells that lost FoxP3 expression and accumulated in regressing tumors. While recombinant IL-2 improved the therapeutic efficacy of CTLA-4 blockade, the decoy IL-2 receptor α (IL-2Rα, sCD25) inhibited the anticancer effects of CTLA-4 blockade. In 262 metastatic melanoma patients receiving ipilimumab, baseline serum concentrations of sCD25 represented an independent indicator of overall survival, with high levels predicting resistance to therapy. Altogether, these results unravel a role for IL-2 and IL-2 receptors in the anticancer activity of CTLA-4 blockade. Importantly, our study provides the first immunologically relevant biomarker, namely elevated serum sCD25, that predicts resistance to CTLA-4 blockade in patients with melanoma.

Published
2015

28. Pembrolizumab plus trastuzumab in trastuzumab-resistant, advanced, HER2-positive breast cancer (PANACEA): a single-arm, multicentre, phase 1b–2 trial

Author

Fumagalli, Debora, Gelber, Richard D, Goulioti, Theodora, Hiltbrunner, Anita, Hui, Rita, Roschitzki, Heidi, Ruepp, Barbara, Boyle, Fran, Stahel, Rolf, Aebi, Stefan, Coates, Alan S, Goldhirsch, Aron, Karlsson, Per, Kössler, Ingrid, Fournarakou, Stamatina, Gasca, Adriana, Pfister, Rita, Ribeli-Hofmann, Sabrina, Weber, Magdelena, Celotto, Daniela, Comune, Carmen, Frapolli, Michela, Sánchez-Hohl, Magdalena, Huang, Hui, Mahoney, Caitlin, Price, Karen, Scott, Karolyn, Shaw, Holly, Fischer, Susan, Greco, Monica, King, Colleen, Andrighetto, Stefania, Piccart-Gebhart, Martine, Findlay, Heather, Jenkins, Michelle, Karantza, Vassiliki, Mejia, Jaime, Schneier, Patrick, Loi, Sherene, Giobbie-Hurder, Anita, Gombos, Andrea, Bachelot, Thomas, Hui, Rina, Curigliano, Giuseppe, Campone, Mario, Biganzoli, Laura, Bonnefoi, Hervé, Jerusalem, Guy, Bartsch, Rupert, Rabaglio-Poretti, Manuela, Kammler, Roswitha, Maibach, Rudolf, Smyth, Mark J, Di Leo, Angelo, Colleoni, Marco, Viale, Giuseppe, Regan, Meredith M, and André, Fabrice

Published
2019
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30. Author Correction: CIS is a potent checkpoint in NK cell–mediated tumor immunity

Author

Delconte, Rebecca B., primary, Kolesnik, Tatiana B., additional, Dagley, Laura F., additional, Rautela, Jai, additional, Shi, Wei, additional, Putz, Eva M., additional, Stannard, Kimberley, additional, Zhang, Jian-Guo, additional, Teh, Charis, additional, Firth, Matt, additional, Ushiki, Takashi, additional, Andoniou, Christopher E., additional, Degli-Esposti, Mariapia A., additional, Sharp, Phillip P., additional, Sanvitale, Caroline E., additional, Infusini, Giuseppe, additional, Liau, Nicholas P. D., additional, Linossi, Edmond M., additional, Burns, Christopher J., additional, Carotta, Sebastian, additional, Gray, Daniel H. D., additional, Seillet, Cyril, additional, Hutchinson, Dana S., additional, Belz, Gabrielle T., additional, Webb, Andrew I., additional, Alexander, Warren S., additional, Li, Shawn S., additional, Bullock, Alex N., additional, Babon, Jeffrey J., additional, Smyth, Mark J., additional, Nicholson, Sandra E., additional, and Huntington, Nicholas D., additional

Published
2023
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38. BRAF-targeted therapy and immune responses to melanoma

Author

Ngiow, Shin Foong, Knight, Deborah A, Ribas, Antoni, McArthur, Grant A, and Smyth, Mark J

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Immunology, Cancer, Vaccine Related, Immunization, 5.1 Pharmaceuticals, Development of treatments and therapeutic interventions, BRAF, checkpoint, immunity, melanoma, T cell, Oncology and carcinogenesis
Abstract

Type I BRAF inhibitors and immunotherapy constitute two new exciting approaches for the treatment of advanced malignant melanoma. We have recently elucidated a role for host C-C chemokine receptor type 2 (CCR2) in the antineoplastic effects of type I BRAF inhibitors in mice, supporting the therapeutic potential of combining BRAF inhibitors with immunotherapy.

Published
2013

39. Sustained Type I interferon signaling as a mechanism of resistance to PD-1 blockade

Author

Jacquelot, Nicolas, Yamazaki, Takahiro, Roberti, Maria P., Duong, Connie P. M., Andrews, Miles C., Verlingue, Loic, Ferrere, Gladys, Becharef, Sonia, Vétizou, Marie, Daillère, Romain, Messaoudene, Meriem, Enot, David P., Stoll, Gautier, Ugel, Stefano, Marigo, Ilaria, Foong Ngiow, Shin, Marabelle, Aurélien, Prevost-Blondel, Armelle, Gaudreau, Pierre-Olivier, Gopalakrishnan, Vancheswaran, Eggermont, Alexander M., Opolon, Paule, Klein, Christophe, Madonna, Gabriele, Ascierto, Paolo A., Sucker, Antje, Schadendorf, Dirk, Smyth, Mark J., Soria, Jean-Charles, Kroemer, Guido, Bronte, Vincenzo, Wargo, Jennifer, and Zitvogel, Laurence

Published
2019
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41. Retraction: CD155 loss enhances tumor suppression via combined host and tumor-intrinsic mechanisms

Author

Li, Xian-Yang, Das, Indrajit, Lepletier, Ailin, Addala, Venkateswar, Bald, Tobias, Stannard, Kimberley, Barkauskas, Deborah, Liu, Jing, Aguilera, Amelia Roman, Takeda, Kazuyoshi, Braun, Matthias, Nakamura, Kyohei, Jacquelin, Sebastien, Lane, Steven W., Teng, Michele W.L., Dougall, William C., and Smyth, Mark J.

Subjects
Health care industry
Abstract

Original citation: J Clin Invest. 2018;128(6):2613-2625. https://doi.org/10.1172/JCI98769. Citation for this retraction: J Clin Invest. 2022;132(6):e159825. https://doi.org/10.1172/JCI159825. QIMR Berghofer Medical Research Institute recently notified the JCI of concerns regarding Figures 4I [...]

Published
2022
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42. Cancer immunoediting by the innate immune system in the absence of adaptive immunity

Author

O’Sullivan, Timothy, Saddawi-Konefka, Robert, Vermi, William, Koebel, Catherine M, Arthur, Cora, White, J Michael, Uppaluri, Ravi, Andrews, Daniel M, Ngiow, Shin Foong, Teng, Michele WL, Smyth, Mark J, Schreiber, Robert D, and Bui, Jack D

Subjects
Cancer, Aetiology, 2.1 Biological and endogenous factors, Inflammatory and immune system, Adaptive Immunity, Animals, CD40 Antigens, Cell Line, Tumor, DNA-Binding Proteins, Genetic Predisposition to Disease, Histocompatibility Antigens Class II, Immunity, Innate, Immunomodulation, Interferon-gamma, Interleukin Receptor Common gamma Subunit, Killer Cells, Natural, Macrophages, Mice, Mice, Knockout, Neoplasms, Phenotype, Sarcoma, Transplantation, Isogeneic, Medical and Health Sciences, Immunology
Abstract

Cancer immunoediting is the process whereby immune cells protect against cancer formation by sculpting the immunogenicity of developing tumors. Although the full process depends on innate and adaptive immunity, it remains unclear whether innate immunity alone is capable of immunoediting. To determine whether the innate immune system can edit tumor cells in the absence of adaptive immunity, we compared the incidence and immunogenicity of 3'methylcholanthrene-induced sarcomas in syngeneic wild-type, RAG2(-/-), and RAG2(-/-)x γc(-/-) mice. We found that innate immune cells could manifest cancer immunoediting activity in the absence of adaptive immunity. This activity required natural killer (NK) cells and interferon γ (IFN-γ), which mediated the induction of M1 macrophages. M1 macrophages could be elicited by administration of CD40 agonists, thereby restoring editing activity in RAG2(-/-)x γc(-/-) mice. Our results suggest that in the absence of adaptive immunity, NK cell production of IFN-γ induces M1 macrophages, which act as important effectors during cancer immunoediting.

Published
2012

43. Cancer immunoediting by the innate immune system in the absence of adaptive immunity.

Author

O'Sullivan, Timothy, Saddawi-Konefka, Robert, Vermi, William, Koebel, Catherine M, Arthur, Cora, White, J Michael, Uppaluri, Ravi, Andrews, Daniel M, Ngiow, Shin Foong, Teng, Michele WL, Smyth, Mark J, Schreiber, Robert D, and Bui, Jack D

Subjects
Killer Cells, Natural, Cell Line, Tumor, Macrophages, Animals, Mice, Knockout, Mice, Neoplasms, Sarcoma, Genetic Predisposition to Disease, DNA-Binding Proteins, Antigens, CD40, Histocompatibility Antigens Class II, Transplantation, Isogeneic, Phenotype, Interleukin Receptor Common gamma Subunit, Immunity, Innate, Interferon-gamma, Adaptive Immunity, Immunomodulation, CD40 Antigens, Cell Line, Tumor, Immunity, Innate, Killer Cells, Natural, Knockout, Transplantation, Isogeneic, Medical and Health Sciences, Immunology
Abstract

Cancer immunoediting is the process whereby immune cells protect against cancer formation by sculpting the immunogenicity of developing tumors. Although the full process depends on innate and adaptive immunity, it remains unclear whether innate immunity alone is capable of immunoediting. To determine whether the innate immune system can edit tumor cells in the absence of adaptive immunity, we compared the incidence and immunogenicity of 3'methylcholanthrene-induced sarcomas in syngeneic wild-type, RAG2(-/-), and RAG2(-/-)x γc(-/-) mice. We found that innate immune cells could manifest cancer immunoediting activity in the absence of adaptive immunity. This activity required natural killer (NK) cells and interferon γ (IFN-γ), which mediated the induction of M1 macrophages. M1 macrophages could be elicited by administration of CD40 agonists, thereby restoring editing activity in RAG2(-/-)x γc(-/-) mice. Our results suggest that in the absence of adaptive immunity, NK cell production of IFN-γ induces M1 macrophages, which act as important effectors during cancer immunoediting.

Published
2012

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

Author

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, and Hölzel, Michael

Published
2017
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50. Th17 plasticity and transition toward a pathogenic cytokine signature are regulated by cyclosporine after allogeneic SCT

Author

Gartlan, Kate H., Varelias, Antiopi, Koyama, Motoko, Robb, Renee J., Markey, Kate A., Chang, Karshing, Wilkinson, Andrew N., Smith, David, Ullah, Md Ashik, Kuns, Rachel D., Raffelt, Neil C., Olver, Stuart D., Lineburg, Katie E., Teal, Bianca E., Cheong, Melody, Teng, Michele W.L., Smyth, Mark J., Tey, Siok-Keen, MacDonald, Kelli P.A., and Hill, Geoffrey R.

Published
2017
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