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2. CD8+ T cell metabolic flexibility elicited by CD28-ARS2 axis-driven alternative splicing of PKM supports antitumor immunity

Author

Holling, G. Aaron, Chavel, Colin A., Sharda, Anand P., Lieberman, Mackenzie M., James, Caitlin M., Lightman, Shivana M., Tong, Jason H., Qiao, Guanxi, Emmons, Tiffany R., Giridharan, Thejaswini, Hou, Shengqi, Intlekofer, Andrew M., Higashi, Richard M., Fan, Teresa W. M., Lane, Andrew N., Eng, Kevin H., Segal, Brahm H., Repasky, Elizabeth A., Lee, Kelvin P., and Olejniczak, Scott H.

Published
2024
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3. Perspectives in Immunotherapy: meeting report from Immunotherapy Bridge (Naples, November 30th–December 1st, 2022)

Author

Ascierto, Paolo A., Avallone, Antonio, Bifulco, Carlo, Bracarda, Sergio, Brody, Joshua D., Emens, Leisha A., Ferris, Robert L., Formenti, Silvia C., Hamid, Omid, Johnson, Douglas B., Kirchhoff, Tomas, Klebanoff, Christopher A., Lesinski, Gregory B., Monette, Anne, Neyns, Bart, Odunsi, Kunle, Paulos, Chrystal M., Powell, Jr., Daniel J., Rezvani, Katayoun, Segal, Brahm H., Singh, Nathan, Sullivan, Ryan J., Fox, Bernard A., and Puzanov, Igor

Published
2023
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6. History of hypertension, heart disease, and diabetes and ovarian cancer patient survival: evidence from the ovarian cancer association consortium

Author

Minlikeeva, Albina N, Freudenheim, Jo L, Cannioto, Rikki A, Szender, J Brian, Eng, Kevin H, Modugno, Francesmary, Ness, Roberta B, LaMonte, Michael J, Friel, Grace, Segal, Brahm H, Odunsi, Kunle, Mayor, Paul, Zsiros, Emese, Schmalfeldt, Barbara, Klapdor, Rüdiger, Dӧrk, Thilo, Hillemanns, Peter, Kelemen, Linda E, Kӧbel, Martin, Steed, Helen, de Fazio, Anna, on behalf of the Australian Ovarian Cancer Study Group, Jordan, Susan J, Nagle, Christina M, Risch, Harvey A, Rossing, Mary Anne, Doherty, Jennifer A, Goodman, Marc T, Edwards, Robert, Matsuo, Keitaro, Mizuno, Mika, Karlan, Beth Y, Kjær, Susanne K, Høgdall, Estrid, Jensen, Allan, Schildkraut, Joellen M, Terry, Kathryn L, Cramer, Daniel W, Bandera, Elisa V, Paddock, Lisa E, Kiemeney, Lambertus A, Massuger, Leon F, Kupryjanczyk, Jolanta, Berchuck, Andrew, Chang-Claude, Jenny, Diergaarde, Brenda, Webb, Penelope M, Moysich, Kirsten B, and on behalf of the Ovarian Cancer Association Consortium

Subjects
Epidemiology, Biomedical and Clinical Sciences, Health Sciences, Oncology and Carcinogenesis, Clinical Research, Cancer, Diabetes, Ovarian Cancer, Rare Diseases, Genetics, Cardiovascular, Detection, screening and diagnosis, 4.1 Discovery and preclinical testing of markers and technologies, Good Health and Well Being, Adrenergic beta-Antagonists, Adult, Aged, Diabetes Mellitus, Disease-Free Survival, Female, Heart Diseases, Humans, Hypertension, Hypoglycemic Agents, Insulin, Middle Aged, Ovarian Neoplasms, Risk, Survival Rate, Ovarian cancer prognosis, Medications, Mortality, Beta blockers, Australian Ovarian Cancer Study Group, Ovarian Cancer Association Consortium, Public Health and Health Services, Oncology and carcinogenesis
Abstract

PurposeSurvival following ovarian cancer diagnosis is generally low; understanding factors related to prognosis could be important to optimize treatment. The role of previously diagnosed comorbidities and use of medications for those conditions in relation to prognosis for ovarian cancer patients has not been studied extensively, particularly according to histological subtype.MethodsUsing pooled data from fifteen studies participating in the Ovarian Cancer Association Consortium, we examined the associations between history of hypertension, heart disease, diabetes, and medications taken for these conditions and overall survival (OS) and progression-free survival (PFS) among patients diagnosed with invasive epithelial ovarian carcinoma. We used Cox proportional hazards regression models adjusted for age and stage to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) overall and within strata of histological subtypes.ResultsHistory of diabetes was associated with increased risk of mortality (n = 7,674; HR = 1.12; 95% CI = 1.01-1.25). No significant mortality associations were observed for hypertension (n = 6,482; HR = 0.95; 95% CI = 0.88-1.02) or heart disease (n = 4,252; HR = 1.05; 95% CI = 0.87-1.27). No association of these comorbidities was found with PFS in the overall study population. However, among patients with endometrioid tumors, hypertension was associated with lower risk of progression (n = 339, HR = 0.54; 95% CI = 0.35-0.84). Comorbidity was not associated with OS or PFS for any of the other histological subtypes. Ever use of beta blockers, oral antidiabetic medications, and insulin was associated with increased mortality, HR = 1.20; 95% CI = 1.03-1.40, HR = 1.28; 95% CI = 1.05-1.55, and HR = 1.63; 95% CI = 1.20-2.20, respectively. Ever use of diuretics was inversely associated with mortality, HR = 0.71; 95% CI = 0.53-0.94.ConclusionsHistories of hypertension, diabetes, and use of diuretics, beta blockers, insulin, and oral antidiabetic medications may influence the survival of ovarian cancer patients. Understanding mechanisms for these observations could provide insight regarding treatment.

Published
2017

7. No Evidence That Genetic Variation in the Myeloid-Derived Suppressor Cell Pathway Influences Ovarian Cancer Survival

Author

Sucheston-Campbell, Lara E, Cannioto, Rikki, Clay, Alyssa I, Etter, John Lewis, Eng, Kevin H, Liu, Song, Battaglia, Sebastiano, Hu, Qiang, Szender, J Brian, Minlikeeva, Albina, Joseph, Janine M, Mayor, Paul, Abrams, Scott I, Segal, Brahm H, Wallace, Paul K, Soh, Kah Teong, Zsiros, Emese, Anton-Culver, Hoda, Bandera, Elisa V, Beckmann, Matthias W, Berchuck, Andrew, Bjorge, Line, Bruegl, Amanda, Campbell, Ian G, Campbell, Shawn Patrice, Chenevix-Trench, Georgia, Study, on behalf of the Australian Ovarian Cancer, Cramer, Daniel W, Dansonka-Mieszkowska, Agnieszka, Dao, Fanny, Diergaarde, Brenda, Doerk, Thilo, Doherty, Jennifer A, du Bois, Andreas, Eccles, Diana, Engelholm, Svend Aage, Fasching, Peter A, Gayther, Simon A, Gentry-Maharaj, Aleksandra, Glasspool, Rosalind M, Goodman, Marc T, Gronwald, Jacek, Harter, Philipp, Hein, Alexander, Heitz, Florian, Hillemmanns, Peter, Høgdall, Claus, Høgdall, Estrid VS, Huzarski, Tomasz, Jensen, Allan, Johnatty, Sharon E, Jung, Audrey, Karlan, Beth Y, Klapdor, Reudiger, Kluz, Tomasz, Konopka, Bożena, Kjær, Susanne Krüger, Kupryjanczyk, Jolanta, Lambrechts, Diether, Lester, Jenny, Lubiński, Jan, Levine, Douglas A, Lundvall, Lene, McGuire, Valerie, McNeish, Iain A, Menon, Usha, Modugno, Francesmary, Ness, Roberta B, Orsulic, Sandra, Paul, James, Pearce, Celeste Leigh, Pejovic, Tanja, Pharoah, Paul, Ramus, Susan J, Rothstein, Joseph, Rossing, Mary Anne, Rübner, Matthias, Schildkraut, Joellen M, Schmalfeldt, Barbara, Schwaab, Ira, Siddiqui, Nadeem, Sieh, Weiva, Sobiczewski, Piotr, Song, Honglin, Terry, Kathryn L, Van Nieuwenhuysen, Els, Vanderstichele, Adriaan, Vergote, Ignace, Walsh, Christine S, Webb, Penelope M, Wentzensen, Nicolas, Whittemore, Alice S, Wu, Anna H, Ziogas, Argyrios, Odunsi, Kunle, Chang-Claude, Jenny, Goode, Ellen L, and Moysich, Kirsten B

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Immunology, Clinical Research, Cancer, Ovarian Cancer, Rare Diseases, Prevention, Genetics, Genetic Testing, 2.1 Biological and endogenous factors, Aetiology, Carcinoma, Ovarian Epithelial, Female, Genetic Association Studies, Genetic Variation, Humans, Myeloid-Derived Suppressor Cells, Neoplasms, Glandular and Epithelial, Ovarian Neoplasms, Australian Ovarian Cancer Study, Medical and Health Sciences, Epidemiology, Biomedical and clinical sciences, Health sciences
Abstract

Background: The precise mechanism by which the immune system is adversely affected in cancer patients remains poorly understood, but the accumulation of immunosuppressive/protumorigenic myeloid-derived suppressor cells (MDSCs) is thought to be a prominent mechanism contributing to immunologic tolerance of malignant cells in epithelial ovarian cancer (EOC). To this end, we hypothesized genetic variation in MDSC pathway genes would be associated with survival after EOC diagnoses.Methods: We measured the hazard of death due to EOC within 10 years of diagnosis, overall and by invasive subtype, attributable to SNPs in 24 genes relevant in the MDSC pathway in 10,751 women diagnosed with invasive EOC. Versatile Gene-based Association Study and the admixture likelihood method were used to test gene and pathway associations with survival.Results: We did not identify individual SNPs that were significantly associated with survival after correction for multiple testing (P < 3.5 × 10-5), nor did we identify significant associations between the MDSC pathway overall, or the 24 individual genes and EOC survival.Conclusions: In this well-powered analysis, we observed no evidence that inherited variations in MDSC-associated SNPs, individual genes, or the collective genetic pathway contributed to EOC survival outcomes.Impact: Common inherited variation in genes relevant to MDSCs was not associated with survival in women diagnosed with invasive EOC. Cancer Epidemiol Biomarkers Prev; 26(3); 420-4. ©2016 AACR.

Published
2017

10. Practice Guidelines for the Diagnosis and Management of Aspergillosis: 2016 Update by the Infectious Diseases Society of America

Author

Patterson, Thomas F, Thompson, George R, Denning, David W, Fishman, Jay A, Hadley, Susan, Herbrecht, Raoul, Kontoyiannis, Dimitrios P, Marr, Kieren A, Morrison, Vicki A, Nguyen, M Hong, Segal, Brahm H, Steinbach, William J, Stevens, David A, Walsh, Thomas J, Wingard, John R, Young, Jo-Anne H, and Bennett, John E

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Rare Diseases, Clinical Research, Management of diseases and conditions, 7.3 Management and decision making, Good Health and Well Being, Amphotericin B, Antifungal Agents, Aspergillosis, Azoles, Echinocandins, Humans, Infectious Disease Medicine, Societies, Medical, United States, aspergillosis, invasive aspergillosis, allergic aspergillosis, chronic aspergillosis, fungal diagnostics, azoles, echniocandins, amphotericin, Biological Sciences, Medical and Health Sciences, Microbiology, Clinical sciences
Abstract

It is important to realize that guidelines cannot always account for individual variation among patients. They are not intended to supplant physician judgment with respect to particular patients or special clinical situations. IDSA considers adherence to these guidelines to be voluntary, with the ultimate determination regarding their application to be made by the physician in the light of each patient's individual circumstances.

Published
2016

11. Executive Summary: Practice Guidelines for the Diagnosis and Management of Aspergillosis: 2016 Update by the Infectious Diseases Society of America

Author

Patterson, Thomas F, Thompson, George R, Denning, David W, Fishman, Jay A, Hadley, Susan, Herbrecht, Raoul, Kontoyiannis, Dimitrios P, Marr, Kieren A, Morrison, Vicki A, Nguyen, M Hong, Segal, Brahm H, Steinbach, William J, Stevens, David A, Walsh, Thomas J, Wingard, John R, Young, Jo-Anne H, and Bennett, John E

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Rare Diseases, Clinical Research, 7.3 Management and decision making, Management of diseases and conditions, Good Health and Well Being, Amphotericin B, Antifungal Agents, Aspergillosis, Azoles, Echinocandins, Humans, Infectious Disease Medicine, Practice Guidelines as Topic, Societies, Medical, United States, aspergillosis, invasive aspergillosis, allergic aspergillosis, chronic aspergillosis, fungal diagnostics, azoles, echniocandins, amphotericin, Biological Sciences, Medical and Health Sciences, Microbiology, Clinical sciences
Abstract

It is important to realize that guidelines cannot always account for individual variation among patients. They are not intended to supplant physician judgment with respect to particular patients or special clinical situations. IDSA considers adherence to these guidelines to be voluntary, with the ultimate determination regarding their application to be made by the physician in the light of each patient's individual circumstances.

Published
2016

14. Anthropometric characteristics and ovarian cancer risk and survival

Author

Minlikeeva, Albina N., Moysich, Kirsten B., Mayor, Paul C., Etter, John L., Cannioto, Rikki A., Ness, Roberta B., Starbuck, Kristen, Edwards, Robert P., Segal, Brahm H., Lele, Sashikant, Odunsi, Kunle, Diergaarde, Brenda, and Modugno, Francesmary

Published
2018

15. Contributors

Author

Abers, Michael S., primary, Babushok, Daria V., additional, Ballow, Mark, additional, Boisson, Bertrand, additional, Bonagura, Vincent Robert, additional, Bonilla, Francisco A., additional, Bosco de Oliveira Filho, João, additional, Boztug, Kaan, additional, Broderick, Lori, additional, Butte, Manish J., additional, Candotti, Fabio, additional, Casanova, Jean-Laurent, additional, Chandrakasan, Shanmuganathan, additional, Condino-Neto, Antonio, additional, Crow, Yanick J., additional, Cunningham-Rundles, Charlotte, additional, Dalm, Virgil A.S.H., additional, de Jesus, Adriana A., additional, de Maio, Emma, additional, de Saint Basile, Geneviève, additional, de Vries, Esther, additional, Dokal, Inderjeet, additional, Duncan, Christopher J.A., additional, Durandy, A., additional, Ehl, Stephan, additional, Etzioni, Amos, additional, Ferguson, Polly J., additional, Fleisher, Thomas A., additional, Forbes-Satter, Lisa R., additional, Frank, Michael M., additional, Freeman, Alexandra F., additional, Frémond, Marie-Louise, additional, Frew, John W., additional, Fusaro, Mathieu, additional, Gambineri, Eleonora, additional, Ganetzky, Rebecca D., additional, Gennery, Andrew R., additional, Goldbach-Mansky, Raphaela, additional, Goldstein, Amy C., additional, Graham, John M., additional, Gupton, Stephanie E., additional, Haddad, Elie, additional, Hambleton, Sophie, additional, Hanson, Eric P., additional, Heimall, Jennifer, additional, Helfrich, Miep, additional, Henrickson, Sarah E., additional, Holland, Steven M., additional, Hsu, Amy P., additional, Jyonouchi, Soma, additional, Kashef, Sara, additional, Kelsen, Judith, additional, Khalil, Maya, additional, Klein, Christoph, additional, Kobrynski, Lisa, additional, Kohn, Donald B., additional, Kracker, S., additional, Krueger, James G., additional, Lavoie, Pascal M., additional, Lehman, Heather K., additional, Leiding, Jennifer W., additional, Lenardo, Michael J., additional, Levy, Ofer, additional, Lim, Allison Pecha, additional, Lionakis, Michail S., additional, Lisco, Andrea, additional, Lougaris, Vassilios, additional, Lugo Reyes, Saul O., additional, Markert, M. Louise, additional, Marsh, Rebecca A., additional, McCarthy, Elizabeth A., additional, Meyts, Isabelle, additional, Milito, Cinzia, additional, Milner, Joshua D., additional, Ming, Jeffrey E., additional, Moshous, Despina, additional, Müller, Ludmila, additional, Navrazhina, Kristina, additional, Nichols, Kim E., additional, Notarangelo, Luigi D., additional, Oksenhendler, Eric, additional, Orange, Jordan S., additional, Paganelli, Roberto, additional, Pawelec, Graham, additional, Pentimalli, Tancredi Massimo, additional, Perez, Elena E., additional, Picard, Capucine, additional, Plebani, Alessandro, additional, Porras, Oscar, additional, Przespolewski, Amanda C., additional, Puel, Anne, additional, Pulvirenti, Federica, additional, Quinti, Isabella, additional, Rezaei, Nima, additional, Rijkers, Ger T., additional, Rosenthal, David Walter, additional, Rosenzweig, Sergio D., additional, Segal, Brahm H., additional, Seppänen, Mikko R.J., additional, Sereti, Irini, additional, Shcherbina, Anna, additional, Sobacchi, Cristina, additional, Squire, Jacqueline D., additional, Stepensky, Polina, additional, Su, Helen C., additional, Sullivan, Kathleen E., additional, Torgerson, Troy R., additional, Uzel, Gulbu, additional, van der Burg, Mirjam, additional, Villa, Anna, additional, Villartay, Jean-Pierre de, additional, Warnatz, Klaus, additional, Wasserman, Richard L., additional, Weemaes, Corry M.R., additional, Yu, Joyce E., additional, Zhang, Shen-Ying, additional, and Ziegler, John B., additional

Published
2020
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18. Mitochondrial DNA in the tumour microenvironment activates neutrophils and is associated with worse outcomes in patients with advanced epithelial ovarian cancer

Author

Singel, Kelly L., Grzankowski, Kassondra S., Khan, A. N. M. Nazmul H., Grimm, Melissa J., D’Auria, Anthony C., Morrell, Kayla, Eng, Kevin H., Hylander, Bonnie, Mayor, Paul C., Emmons, Tiffany R., Lénárt, Nikolett, Fekete, Rebeka, Környei, Zsuzsanna, Muthukrishnan, Uma, Gilthorpe, Jonathan D., Urban, Constantin F., Itagaki, Kiyoshi, Hauser, Carl J., Leifer, Cynthia, Moysich, Kirsten B., Odunsi, Kunle, Dénes, Ádám, and Segal, Brahm H.

Published
2019
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19. Tracing Conidial Fate and Measuring Host Cell Antifungal Activity Using a Reporter of Microbial Viability in the Lung

Author

Jhingran, Anupam, Mar, Katrina B, Kumasaka, Debra K, Knoblaugh, Sue E, Ngo, Lisa Y, Segal, Brahm H, Iwakura, Yoichiro, Lowell, Clifford A, Hamerman, Jessica A, Lin, Xin, and Hohl, Tobias M

Subjects
Microbiology, Biological Sciences, Biodefense, Emerging Infectious Diseases, Lung, Prevention, Infectious Diseases, Vaccine Related, Aetiology, 2.2 Factors relating to the physical environment, 2.1 Biological and endogenous factors, Infection, Adaptor Proteins, Signal Transducing, Animals, Aspergillosis, Aspergillus fumigatus, CARD Signaling Adaptor Proteins, Host-Pathogen Interactions, Immunity, Innate, Intracellular Signaling Peptides and Proteins, Mice, Mice, Knockout, Pneumonia, Protein-Tyrosine Kinases, Spores, Fungal, Syk Kinase, Biochemistry and Cell Biology, Medical Physiology, Biological sciences
Abstract

Fluorescence can be harnessed to monitor microbial fate and to investigate functional outcomes of individual microbial cell-host cell encounters at portals of entry in native tissue environments. We illustrate this concept by introducing fluorescent Aspergillus reporter (FLARE) conidia that simultaneously report phagocytic uptake and fungal viability during cellular interactions with the murine respiratory innate immune system. Our studies using FLARE conidia reveal stepwise and cell-type-specific requirements for CARD9 and Syk, transducers of C-type lectin receptor and integrin signals, in neutrophil recruitment, conidial uptake, and conidial killing in the lung. By achieving single-event resolution in defined leukocyte populations, the FLARE method enables host cell profiling on the basis of pathogen uptake and killing and may be extended to other pathogens in diverse model host organisms to query molecular, cellular, and pharmacologic mechanisms that shape host-microbe interactions.

Published
2012

20. NADPH oxidase limits innate immune responses in the lungs in mice.

Author

Segal, Brahm H, Han, Wei, Bushey, Jennifer J, Joo, Myungsoo, Bhatti, Zahida, Feminella, Joy, Dennis, Carly G, Vethanayagam, R Robert, Yull, Fiona E, Capitano, Maegan, Wallace, Paul K, Minderman, Hans, Christman, John W, Sporn, Michael B, Chan, Jefferson, Vinh, Donald C, Holland, Steven M, Romani, Luigina R, Gaffen, Sarah L, Freeman, Michael L, and Blackwell, Timothy S

Subjects
Lung, Macrophages, Animals, Mice, Granulomatous Disease, Chronic, Inflammation, NF-kappa B, Membrane Glycoproteins, Cytokines, Gene Expression Regulation, Enzymologic, Oxidation-Reduction, NF-E2-Related Factor 2, Immunity, Innate, NADPH Oxidase 2, NADPH Oxidases, Granulomatous Disease, Chronic, NADPH Oxidase, Gene Expression Regulation, Enzymologic, Immunity, Innate, General Science & Technology
Abstract

BackgroundChronic granulomatous disease (CGD), an inherited disorder of the NADPH oxidase in which phagocytes are defective in generating superoxide anion and downstream reactive oxidant intermediates (ROIs), is characterized by recurrent bacterial and fungal infections and by excessive inflammation (e.g., inflammatory bowel disease). The mechanisms by which NADPH oxidase regulates inflammation are not well understood.Methodology/principal findingsWe found that NADPH oxidase restrains inflammation by modulating redox-sensitive innate immune pathways. When challenged with either intratracheal zymosan or LPS, NADPH oxidase-deficient p47(phox-/-) mice and gp91(phox)-deficient mice developed exaggerated and progressive lung inflammation, augmented NF-kappaB activation, and elevated downstream pro-inflammatory cytokines (TNF-alpha, IL-17, and G-CSF) compared to wildtype mice. Replacement of functional NADPH oxidase in bone marrow-derived cells restored the normal lung inflammatory response. Studies in vivo and in isolated macrophages demonstrated that in the absence of functional NADPH oxidase, zymosan failed to activate Nrf2, a key redox-sensitive anti-inflammatory regulator. The triterpenoid, CDDO-Im, activated Nrf2 independently of NADPH oxidase and reduced zymosan-induced lung inflammation in CGD mice. Consistent with these findings, zymosan-treated peripheral blood mononuclear cells from X-linked CGD patients showed impaired Nrf2 activity and increased NF-kappaB activation.Conclusions/significanceThese studies support a model in which NADPH oxidase-dependent, redox-mediated signaling is critical for termination of lung inflammation and suggest new potential therapeutic targets for CGD.

Published
2010

22. Neutrophils in the tumor microenvironment (TME) induce T cell non-responsiveness characterized by a shift from proliferation and activation to lipid transport pathways.

Author

Giridharan, Thejaswini, primary, Suzuki, Sora, additional, Khan, ANM Nazmul H., additional, Stokolosa, Anna, additional, Long, Mark D., additional, Rosario, Spencer R., additional, Emmons, Tiffany R., additional, Yaffe, Michael B., additional, Zsiros, Emese, additional, and Segal, Brahm H., additional

Published
2023
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25. Data from Quantification of Early-Stage Myeloid-Derived Suppressor Cells in Cancer Requires Excluding Basophils

Author

Khan, ANM Nazmul H., primary, Emmons, Tiffany R., primary, Wong, Jerry T., primary, Alqassim, Emad, primary, Singel, Kelly L., primary, Mark, Jaron, primary, Smith, Brandon E., primary, Tario, Joseph D., primary, Eng, Kevin H., primary, Moysich, Kirsten B., primary, Odunsi, Kunle, primary, Abrams, Scott I., primary, and Segal, Brahm H., primary

Published
2023
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26. Supplementary Tables from Mechanisms Driving Neutrophil-Induced T-cell Immunoparalysis in Ovarian Cancer

Author

Emmons, Tiffany R., primary, Giridharan, Thejaswini, primary, Singel, Kelly L., primary, Khan, ANM Nazmul H., primary, Ricciuti, Jason, primary, Howard, Kaitlyn, primary, Silva-Del Toro, Stephanie L., primary, Debreceni, Ivy L., primary, Aarts, Cathelijn E.M., primary, Brouwer, Mieke C., primary, Suzuki, Sora, primary, Kuijpers, Taco W., primary, Jongerius, Ilse, primary, Allen, Lee-Ann H., primary, Ferreira, Viviana P., primary, Schubart, Anna, primary, Sellner, Holger, primary, Eder, Jörg, primary, Holland, Steven M., primary, Ram, Sanjay, primary, Lederer, James A., primary, Eng, Kevin H., primary, Moysich, Kirsten B., primary, Odunsi, Kunle, primary, Yaffe, Michael B., primary, Zsiros, Emese, primary, and Segal, Brahm H., primary

Published
2023
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27. Supplementary Figure S4 from Mechanisms Driving Neutrophil-Induced T-cell Immunoparalysis in Ovarian Cancer

Author

Emmons, Tiffany R., primary, Giridharan, Thejaswini, primary, Singel, Kelly L., primary, Khan, ANM Nazmul H., primary, Ricciuti, Jason, primary, Howard, Kaitlyn, primary, Silva-Del Toro, Stephanie L., primary, Debreceni, Ivy L., primary, Aarts, Cathelijn E.M., primary, Brouwer, Mieke C., primary, Suzuki, Sora, primary, Kuijpers, Taco W., primary, Jongerius, Ilse, primary, Allen, Lee-Ann H., primary, Ferreira, Viviana P., primary, Schubart, Anna, primary, Sellner, Holger, primary, Eder, Jörg, primary, Holland, Steven M., primary, Ram, Sanjay, primary, Lederer, James A., primary, Eng, Kevin H., primary, Moysich, Kirsten B., primary, Odunsi, Kunle, primary, Yaffe, Michael B., primary, Zsiros, Emese, primary, and Segal, Brahm H., primary

Published
2023
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28. Data from Mechanisms Driving Neutrophil-Induced T-cell Immunoparalysis in Ovarian Cancer

Author

Emmons, Tiffany R., primary, Giridharan, Thejaswini, primary, Singel, Kelly L., primary, Khan, ANM Nazmul H., primary, Ricciuti, Jason, primary, Howard, Kaitlyn, primary, Silva-Del Toro, Stephanie L., primary, Debreceni, Ivy L., primary, Aarts, Cathelijn E.M., primary, Brouwer, Mieke C., primary, Suzuki, Sora, primary, Kuijpers, Taco W., primary, Jongerius, Ilse, primary, Allen, Lee-Ann H., primary, Ferreira, Viviana P., primary, Schubart, Anna, primary, Sellner, Holger, primary, Eder, Jörg, primary, Holland, Steven M., primary, Ram, Sanjay, primary, Lederer, James A., primary, Eng, Kevin H., primary, Moysich, Kirsten B., primary, Odunsi, Kunle, primary, Yaffe, Michael B., primary, Zsiros, Emese, primary, and Segal, Brahm H., primary

Published
2023
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29. Supplementary Data Table S1 from Quantification of Early-Stage Myeloid-Derived Suppressor Cells in Cancer Requires Excluding Basophils

Author

Khan, ANM Nazmul H., primary, Emmons, Tiffany R., primary, Wong, Jerry T., primary, Alqassim, Emad, primary, Singel, Kelly L., primary, Mark, Jaron, primary, Smith, Brandon E., primary, Tario, Joseph D., primary, Eng, Kevin H., primary, Moysich, Kirsten B., primary, Odunsi, Kunle, primary, Abrams, Scott I., primary, and Segal, Brahm H., primary

Published
2023
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30. Supplementary Data Figure S1 from Quantification of Early-Stage Myeloid-Derived Suppressor Cells in Cancer Requires Excluding Basophils

Author

Khan, ANM Nazmul H., primary, Emmons, Tiffany R., primary, Wong, Jerry T., primary, Alqassim, Emad, primary, Singel, Kelly L., primary, Mark, Jaron, primary, Smith, Brandon E., primary, Tario, Joseph D., primary, Eng, Kevin H., primary, Moysich, Kirsten B., primary, Odunsi, Kunle, primary, Abrams, Scott I., primary, and Segal, Brahm H., primary

Published
2023
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31. Data from Predictive and Prognostic Implications of Circulating CX3CR1+ CD8+ T Cells in Non–Small Cell Lung Cancer Patients Treated with Chemo-Immunotherapy

Author

Abdelfatah, Eihab, primary, Long, Mark D., primary, Kajihara, Ryutaro, primary, Oba, Takaaki, primary, Yamauchi, Takayoshi, primary, Chen, Hongbin, primary, Sarkar, Joy, primary, Attwood, Kristopher, primary, Matsuzaki, Junko, primary, Segal, Brahm H., primary, Dy, Grace K., primary, and Ito, Fumito, primary

Published
2023
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32. Supplementary Figure S6 from Predictive and Prognostic Implications of Circulating CX3CR1+ CD8+ T Cells in Non–Small Cell Lung Cancer Patients Treated with Chemo-Immunotherapy

Author

Abdelfatah, Eihab, primary, Long, Mark D., primary, Kajihara, Ryutaro, primary, Oba, Takaaki, primary, Yamauchi, Takayoshi, primary, Chen, Hongbin, primary, Sarkar, Joy, primary, Attwood, Kristopher, primary, Matsuzaki, Junko, primary, Segal, Brahm H., primary, Dy, Grace K., primary, and Ito, Fumito, primary

Published
2023
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33. Supplementary Tables S1-9 from Predictive and Prognostic Implications of Circulating CX3CR1+ CD8+ T Cells in Non–Small Cell Lung Cancer Patients Treated with Chemo-Immunotherapy

Author

Abdelfatah, Eihab, primary, Long, Mark D., primary, Kajihara, Ryutaro, primary, Oba, Takaaki, primary, Yamauchi, Takayoshi, primary, Chen, Hongbin, primary, Sarkar, Joy, primary, Attwood, Kristopher, primary, Matsuzaki, Junko, primary, Segal, Brahm H., primary, Dy, Grace K., primary, and Ito, Fumito, primary

Published
2023
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34. Predictive and Prognostic Implications of Circulating CX3CR1+ CD8+ T cells in Non-Small Cell Lung Cancer Patients Treated with Chemo-Immunotherapy

Author

Abdelfatah, Eihab, primary, Long, Mark D, additional, Kajihara, Ryutaro, additional, Oba, Takaaki, additional, Yamauchi, Takayoshi, additional, Chen, Hongbin, additional, Sarkar, Joy, additional, Attwood, Kristopher, additional, Matsuzaki, Junko, additional, Segal, Brahm H, additional, Dy, Grace K., additional, and Ito, Fumito, additional

Published
2023
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35. Postoperative Restrictive Opioid Protocols and Durable Changes in Opioid Prescribing and Chronic Opioid Use

Author

Zsiros, Emese, primary, Ricciuti, Jason, additional, Gallo, Steven, additional, Argentieri, Deanna, additional, Attwood, Kristopher, additional, Ji, Wenyan, additional, Hutson, Alan, additional, Visco, Paul, additional, Coffey, Devon, additional, Riebandt, Grazyna, additional, Mark, Jaron, additional, Varghese, Aaron, additional, Hess, Suzanne M., additional, Furlani, Thomas, additional, Fabiano, Andrew, additional, Hennon, Mark, additional, Yendamuri, Sai, additional, Kauffman, Eric C., additional, Wooten, Kimberly E., additional, Hicks, Wesley L., additional, Young, Jessica, additional, Takabe, Kazuaki, additional, Odunsi, Kunle, additional, Case, Amy A., additional, Segal, Brahm H., additional, Johnson, Candace S., additional, Kuvshinoff, Boris, additional, Nurkin, Steven, additional, Paragh, Gyorgy, additional, and de Leon-Casasola, Oscar, additional

Published
2023
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40. Neutrophil interactions with T cells, platelets, endothelial cells, and of course tumor cells

Author

Segal, Brahm H., primary, Giridharan, Thejaswini, additional, Suzuki, Sora, additional, Khan, ANM Nazmul H., additional, Zsiros, Emese, additional, Emmons, Tiffany R., additional, Yaffe, Michael B., additional, Gankema, Angela A. F., additional, Hoogeboom, Mark, additional, Goetschalckx, Ines, additional, Matlung, Hanke L., additional, and Kuijpers, Taco W., additional

Published
2022
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43. Neutrophil heterogeneity and emergence of a distinct population of CD11b/CD18-activated low-density neutrophils after trauma

Author

Goretti Riça, Ingred, primary, Joughin, Brian A., additional, Teke, Martha E., additional, Emmons, Tiffany R., additional, Griffith, Alec M., additional, Cahill, Laura A., additional, Banner-Goodspeed, Valerie M., additional, Robson, Simon C., additional, Hernandez, Jonathan M., additional, Segal, Brahm H., additional, Otterbein, Leo E., additional, Hauser, Carl J., additional, Lederer, James A., additional, and Yaffe, Michael B., additional

Published
2022
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50. Mechanisms Driving Neutrophil-Induced T-cell Immunoparalysis in Ovarian Cancer

Author

Emmons, Tiffany R., Giridharan, Thejaswini, Singel, Kelly L., Khan, ANM Nazmul H., Ricciuti, Jason, Howard, Kaitlyn, Silva-Del Toro, Stephanie L., Debreceni, Ivy L., Aarts, Cathelijn E.M., Brouwer, Mieke C., Suzuki, Sora, Kuijpers, Taco W., Jongerius, Ilse, Allen, Lee-Ann H., Ferreira, Viviana P., Schubart, Anna, Sellner, Holger, Eder, Jörg, Holland, Steven M., Ram, Sanjay, Lederer, James A., Eng, Kevin H., Moysich, Kirsten B., Odunsi, Kunle, Yaffe, Michael B., Zsiros, Emese, Segal, Brahm H., Emmons, Tiffany R., Giridharan, Thejaswini, Singel, Kelly L., Khan, ANM Nazmul H., Ricciuti, Jason, Howard, Kaitlyn, Silva-Del Toro, Stephanie L., Debreceni, Ivy L., Aarts, Cathelijn E.M., Brouwer, Mieke C., Suzuki, Sora, Kuijpers, Taco W., Jongerius, Ilse, Allen, Lee-Ann H., Ferreira, Viviana P., Schubart, Anna, Sellner, Holger, Eder, Jörg, Holland, Steven M., Ram, Sanjay, Lederer, James A., Eng, Kevin H., Moysich, Kirsten B., Odunsi, Kunle, Yaffe, Michael B., Zsiros, Emese, and Segal, Brahm H.

Abstract

T-cell activation and expansion in the tumor microenvironment (TME) are critical for antitumor immunity. Neutrophils in the TME acquire a complement-dependent T-cell suppressor phenotype that is characterized by inhibition of T-cell proliferation and activation through mechanisms distinct from those of myeloid-derived suppressor cells. In this study, we used ascites fluid supernatants (ASC) from patients with ovarian cancer as an authentic component of the TME to evaluate the effects of ASC on neutrophil function and mechanisms for neutrophil-driven immune suppression. ASC prolonged neutrophil life span, decreased neutrophil density, and induced nuclear hypersegmentation. Mass cytometry analysis showed that ASC induced 15 distinct neutrophil clusters. ASC stimulated complement deposition and signaling in neutrophils, resulting in surface mobilization of granule constituents, including NADPH oxidase. NADPH oxidase activation and phosphatidylserine signaling were required for neutrophil suppressor function, although we did not observe a direct role of extracellular reactive oxygen species in inhibiting T-cell proliferation. Postoperative surgical drainage fluid also induced a complement-dependent neutrophil suppressor phenotype, pointing to this effect as a general response to injury. Like circulating lymphocytes, ASC-activated neutrophils caused complement-dependent suppression of tumor-associated lymphocytes. ASC-activated neutrophils adhered to T cells and caused trogocytosis of T-cell membranes. These injury and signaling cues resulted in T-cell immunoparalysis characterized by impaired NFAT translocation, IL2 production, glucose uptake, mitochondrial function, and mTOR activation. Our results demonstrate that complement-dependent priming of neutrophil effector functions in the TME induces a T-cell nonresponsiveness distinct from established checkpoint pathways and identify targets for immunotherapy.See related Spotlight by Cassatella, p. 725.

Published
2022

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