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2. Obesity induces PD-1 on macrophages to suppress anti-tumour immunity

Author

Bader, Jackie E., Wolf, Melissa M., Lupica-Tondo, Gian Luca, Madden, Matthew Z., Reinfeld, Bradley I., Arner, Emily N., Hathaway, Emma S., Steiner, KayLee K., Needle, Gabriel A., Hatem, Zaid, Landis, Madelyn D., Faneuff, Eden E., Blackman, Amondrea, Wolf, Elysa M., Cottam, Matthew A., Ye, Xiang, Bates, Madison E., Smart, Kyra, Wang, Wenjun, Pinheiro, Laura V., Christofides, Anthos, Smith, DuPreez, Boussiotis, Vassiliki A., Haake, Scott M., Beckermann, Kathryn E., Wellen, Kathryn E., Reinhart-King, Cynthia A., Serezani, C. Henrique, Lee, Cheng-Han, Aubrey, Christa, Chen, Heidi, Rathmell, W. Kimryn, Hasty, Alyssa H., and Rathmell, Jeffrey C.

Published
2024
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3. Author Correction: Obesity induces PD-1 on macrophages to suppress anti-tumour immunity

Author

Bader, Jackie E., Wolf, Melissa M., Lupica-Tondo, Gian Luca, Madden, Matthew Z., Reinfeld, Bradley I., Arner, Emily N., Hathaway, Emma S., Steiner, KayLee K., Needle, Gabriel A., Hatem, Zaid, Landis, Madelyn D., Faneuff, Eden E., Blackman, Amondrea, Wolf, Elysa M., Cottam, Matthew A., Ye, Xiang, Bates, Madison E., Smart, Kyra, Wang, Wenjun, Pinheiro, Laura V., Christofides, Anthos, Smith, DuPreez, Boussiotis, Vassiliki A., Haake, Scott M., Beckermann, Kathryn E., Wellen, Kathryn E., Reinhart-King, Cynthia A., Serezani, C. Henrique, Lee, Cheng-Han, Aubrey, Christa, Chen, Heidi, Rathmell, W. Kimryn, Hasty, Alyssa H., and Rathmell, Jeffrey C.

Published
2024
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5. The glucose transporter 2 regulates CD8+ T cell function via environment sensing

Author

Fu, Hongmei, Vuononvirta, Juho, Fanti, Silvia, Bonacina, Fabrizia, D’Amati, Antonio, Wang, Guosu, Poobalasingam, Thanushiyan, Fankhaenel, Maria, Lucchesi, Davide, Coleby, Rachel, Tarussio, David, Thorens, Bernard, Hearnden, Robert J., Longhi, M. Paula, Grevitt, Paul, Sheikh, Madeeha H., Solito, Egle, Godinho, Susana A., Bombardieri, Michele, Smith, David M., Cooper, Dianne, Iqbal, Asif J., Rathmell, Jeffrey C., Schaefer, Samuel, Morales, Valle, Bianchi, Katiuscia, Norata, Giuseppe Danilo, and Marelli-Berg, Federica M.

Published
2023
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6. T cells specific for α-myosin drive immunotherapy-related myocarditis

Author

Axelrod, Margaret L, Meijers, Wouter C, Screever, Elles M, Qin, Juan, Carroll, Mary Grace, Sun, Xiaopeng, Tannous, Elie, Zhang, Yueli, Sugiura, Ayaka, Taylor, Brandie C, Hanna, Ann, Zhang, Shaoyi, Amancherla, Kaushik, Tai, Warren, Wright, Jordan J, Wei, Spencer C, Opalenik, Susan R, Toren, Abigail L, Rathmell, Jeffrey C, Ferrell, P Brent, Phillips, Elizabeth J, Mallal, Simon, Johnson, Douglas B, Allison, James P, Moslehi, Javid J, and Balko, Justin M

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Immunology, Cardiovascular, Heart Disease, Aetiology, 2.1 Biological and endogenous factors, Inflammatory and immune system, Animals, Mice, Autoantigens, CD8-Positive T-Lymphocytes, CTLA-4 Antigen, Immunotherapy, Myocarditis, Ventricular Myosins, General Science & Technology
Abstract

Immune-related adverse events, particularly severe toxicities such as myocarditis, are major challenges to the utility of immune checkpoint inhibitors (ICIs) in anticancer therapy1. The pathogenesis of ICI-associated myocarditis (ICI-MC) is poorly understood. Pdcd1-/-Ctla4+/- mice recapitulate clinicopathological features of ICI-MC, including myocardial T cell infiltration2. Here, using single-cell RNA and T cell receptor (TCR) sequencing of cardiac immune infiltrates from Pdcd1-/-Ctla4+/- mice, we identify clonal effector CD8+ T cells as the dominant cell population. Treatment with anti-CD8-depleting, but not anti-CD4-depleting, antibodies improved the survival of Pdcd1-/-Ctla4+/- mice. Adoptive transfer of immune cells from mice with myocarditis induced fatal myocarditis in recipients, which required CD8+ T cells. The cardiac-specific protein α-myosin, which is absent from the thymus3,4, was identified as the cognate antigen source for three major histocompatibility complex class I-restricted TCRs derived from mice with fulminant myocarditis. Peripheral blood T cells from three patients with ICI-MC were expanded by α-myosin peptides. Moreover, these α-myosin-expanded T cells shared TCR clonotypes with diseased heart and skeletal muscle, which indicates that α-myosin may be a clinically important autoantigen in ICI-MC. These studies underscore the crucial role for cytotoxic CD8+ T cells, identify a candidate autoantigen in ICI-MC and yield new insights into the pathogenesis of ICI toxicity.

Published
2022

7. HIF-2[alpha] expression and metabolic signaling require ACSS2 in clear cell renal cell carcinoma

Author

Bacigalupa, Zachary A., Arner, Emily N., Vlach, Logan M., Wolf, Melissa M., Brown, Whitney A., Krystofiak, Evan S., Ye, Xiang, Hongo, Rachel A., Landis, Madelyn, Amason, Edith K., Beckermann, Kathryn E., Rathmell, W. Kimryn, and Rathmell, Jeffrey C.

Subjects
Oncology, Experimental, Gene expression -- Research, Cell metabolism -- Research, Carcinoma, Renal cell -- Development and progression -- Genetic aspects, Cellular signal transduction -- Research, Cancer -- Research, Transcription factors -- Health aspects -- Genetic aspects, Health care industry
Abstract

Clear cell renal cell carcinoma (ccRCC) is an aggressive cancer driven by VHL loss and aberrant HIF-2[alpha] signaling. Identifying means to regulate HIF-2[alpha] thus has potential therapeutic benefit. Acetyl- CoA synthetase 2 (ACSS2) converts acetate to acetyl-CoA and is associated with poor patient prognosis in ccRCC. Here we tested the effects of ACSS2 on HIF-2[alpha] and cancer cell metabolism and growth in ccRCC models and clinical samples. ACSS2 inhibition reduced HIF-2[alpha] levels and suppressed ccRCC cell line growth in vitro, in vivo, and in cultures of primary ccRCC patient tumors. This treatment reduced glycolytic signaling, cholesterol metabolism, and mitochondrial integrity, all of which are consistent with loss of HIF-2[alpha]. Mechanistically, ACSS2 inhibition decreased chromatin accessibility and HIF- 2[alpha] expression and stability. While HIF-2[alpha] protein levels are widely regulated through pVHL-dependent proteolytic degradation, we identify a potential pVHLindependent pathway of degradation via the E3 ligase MUL1. We show that MUL1 can directly interact with HIF-2[alpha] and that overexpression of MUL1 decreased HIF-2[alpha] levels in a manner partially dependent on ACSS2. These findings identify multiple mechanisms to regulate HIF-2[alpha] stability and ACSS2 inhibition as a strategy to complement HIF-2[alpha]-targeted therapies and deplete pathogenically stabilized HIF-2[alpha]., Introduction Clear cell renal cell carcinoma (ccRCC) is the most abundant subtype of kidney cancer, accounting for 75% of all cases (1). In ccRCC, a deregulated hypoxia transcriptional response is [...]

Published
2024
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8. VHL loss reprograms the immune landscape to promote an inflammatory myeloid microenvironment in renal tumorigenesis

Author

Wolf, Melissa M., Madden, Matthew Z., Arner, Emily N., Bader, Jackie E., Ye, Xiang, Vlach, Logan, Tigue, Megan L., Landis, Madelyn D., Jonker, Patrick B., Hatem, Zaid, Steiner, KayLee K., Gaines, Dakim K., Reinfeld, Bradley I., Hathaway, Emma S., Xin, Fuxue, Tantawy, M. Noor, Haake, Scott M., Jonasch, Eric, Muir, Alexander, Weiss, Vivian L., Beckermann, Kathryn E., Rathmell, W. Kimryn, and Rathmell, Jeffrey C.

Subjects
United States. National Cancer Institute, Thermo Fisher Scientific Inc., Cell death, Scientific equipment and supplies industry, Tumors, Dextrose, B cells, Glucose, Macrophages, Health care industry, Vanderbilt University. Medical Center
Abstract

Clear cell renal cell carcinoma (ccRCC) is characterized by dysregulated hypoxia signaling and a tumor microenvironment (TME) highly enriched in myeloid and lymphoid cells. Loss of the von Hippel Lindau (VHL) gene is a critical early event in ccRCC pathogenesis and promotes stabilization of HIF. Whether VHL loss in cancer cells affects immune cells in the TME remains unclear. Using Vhl WT and Vhl-KO in vivo murine kidney cancer Renca models, we found that Vhl-KO tumors were more infiltrated by immune cells. Tumor-associated macrophages (TAMs) from Vhl-deficient tumors demonstrated enhanced in vivo glucose consumption, phagocytosis, and inflammatory transcriptional signatures, whereas lymphocytes from Vhl-KO tumors showed reduced activation and a lower response to anti- programmed cell death 1 (anti-PD-1) therapy in vivo. The chemokine CX3CL1 was highly expressed in human ccRCC tumors and was associated with Vhl deficiency. Deletion of Cx3cl1 in cancer cells decreased myeloid cell infiltration associated with Vhl loss to provide a mechanism by which Vhl loss may have contributed to the altered immune landscape. Here, we identify cancer cell-specific genetic features that drove environmental reprogramming and shaped the tumor immune landscape, with therapeutic implications for the treatment of ccRCC., Introduction Clear cell renal cell carcinoma (ccRCC) represents the most frequent subtype of RCC, accounting for approximately 75% of adult clinical cases (1, 2). ccRCC biology is unique due to [...]

Published
2024
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10. High-fat diet–induced colonocyte dysfunction escalates microbiota-derived trimethylamine N-oxide

Author

Yoo, Woongjae, Zieba, Jacob K, Foegeding, Nora J, Torres, Teresa P, Shelton, Catherine D, Shealy, Nicolas G, Byndloss, Austin J, Cevallos, Stephanie A, Gertz, Erik, Tiffany, Connor R, Thomas, Julia D, Litvak, Yael, Nguyen, Henry, Olsan, Erin E, Bennett, Brian J, Rathmell, Jeffrey C, Major, Amy S, Bäumler, Andreas J, and Byndloss, Mariana X

Subjects
Ecological Applications, Biomedical and Clinical Sciences, Biological Sciences, Microbiology, Environmental Sciences, Nutrition, Obesity, Dietary Supplements, Microbiome, Digestive Diseases, Aetiology, 2.1 Biological and endogenous factors, Metabolic and endocrine, Cardiovascular, Oral and gastrointestinal, Animals, Cell Hypoxia, Choline, Colon, Diet, High-Fat, Energy Metabolism, Epithelial Cells, Escherichia coli, Feces, Gastrointestinal Microbiome, Inflammation, Intestinal Mucosa, Male, Methylamines, Mice, Mice, Inbred C57BL, Mitochondria, Nitrates, Oxygen Consumption, General Science & Technology
Abstract

A Western-style, high-fat diet promotes cardiovascular disease, in part because it is rich in choline, which is converted to trimethylamine (TMA) by the gut microbiota. However, whether diet-induced changes in intestinal physiology can alter the metabolic capacity of the microbiota remains unknown. Using a mouse model of diet-induced obesity, we show that chronic exposure to a high-fat diet escalates Escherichia coli choline catabolism by altering intestinal epithelial physiology. A high-fat diet impaired the bioenergetics of mitochondria in the colonic epithelium to increase the luminal bioavailability of oxygen and nitrate, thereby intensifying respiration-dependent choline catabolism of E. coli In turn, E. coli choline catabolism increased levels of circulating trimethlamine N-oxide, which is a potentially harmful metabolite generated by gut microbiota.

Published
2021

11. Single-cell analysis by mass cytometry reveals metabolic states of early-activated CD8+ T cells during the primary immune response

Author

Levine, Lauren S, Hiam-Galvez, Kamir J, Marquez, Diana M, Tenvooren, Iliana, Madden, Matthew Z, Contreras, Diana C, Dahunsi, Debolanle O, Irish, Jonathan M, Oluwole, Olalekan O, Rathmell, Jeffrey C, and Spitzer, Matthew H

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Immunology, Vaccine Related, Rare Diseases, Digestive Diseases, Lymphoma, Prevention, Emerging Infectious Diseases, Cancer, Hematology, Biodefense, 1.1 Normal biological development and functioning, 2.1 Biological and endogenous factors, Underpinning research, Aetiology, Inflammatory and immune system, Animals, CD8-Positive T-Lymphocytes, Cell Proliferation, Female, Glycolysis, Immunologic Memory, Listeria monocytogenes, Listeriosis, Lymphocyte Activation, Mice, Mice, Inbred C57BL, Mice, Transgenic, Oxidative Phosphorylation, Receptors, Chimeric Antigen, Signal Transduction, Single-Cell Analysis, CD8 T cell, T cell activation, immunometabolism, mass cytometry
Abstract

Memory T cells are thought to rely on oxidative phosphorylation and short-lived effector T cells on glycolysis. Here, we investigated how T cells arrive at these states during an immune response. To understand the metabolic state of rare, early-activated T cells, we adapted mass cytometry to quantify metabolic regulators at single-cell resolution in parallel with cell signaling, proliferation, and effector function. We interrogated CD8+ T cell activation in vitro and in response to Listeria monocytogenes infection in vivo. This approach revealed a distinct metabolic state in early-activated T cells characterized by maximal expression of glycolytic and oxidative metabolic proteins. Cells in this transient state were most abundant 5 days post-infection before rapidly decreasing metabolic protein expression. Analogous findings were observed in chimeric antigen receptor (CAR) T cells interrogated longitudinally in advanced lymphoma patients. Our study demonstrates the utility of single-cell metabolic analysis by mass cytometry to identify metabolic adaptations of immune cell populations in vivo and provides a resource for investigations of metabolic regulation of immune responses across a variety of applications.

Published
2021

13. Neurons require glucose uptake and glycolysis in vivo

Author

Li, Huihui, Guglielmetti, Caroline, Sei, Yoshitaka J., Zilberter, Misha, Le Page, Lydia M., Shields, Lauren, Yang, Joyce, Nguyen, Kevin, Tiret, Brice, Gao, Xiao, Bennett, Neal, Lo, Iris, Dayton, Talya L., Kampmann, Martin, Huang, Yadong, Rathmell, Jeffrey C., Vander Heiden, Matthew, Chaumeil, Myriam M., and Nakamura, Ken

Published
2023
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16. Retinoic acid signaling acts as a rheostat to balance Treg function

Author

Thangavelu, Govindarajan, Andrejeva, Gabriela, Bolivar-Wagers, Sara, Jin, Sujeong, Zaiken, Michael C., Loschi, Michael, Aguilar, Ethan G., Furlan, Scott N., Brown, Chrysothemis C., Lee, Yu-Chi, Hyman, Cameron McDonald, Feser, Colby J., Panoskaltsis-Mortari, Angela, Hippen, Keli L., MacDonald, Kelli P., Murphy, William J., Maillard, Ivan, Hill, Geoffrey R., Munn, David H., Zeiser, Robert, Kean, Leslie S., Rathmell, Jeffrey C., Chi, Hongbo, Noelle, Randolph J., and Blazar, Bruce R.

Published
2022
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18. Molecular and clinical characterization of a founder mutation causing G6PC3 deficiency

Author

Zhen, Xin, primary, Betti, Michael J, additional, Kars, Meltem Ece, additional, Patterson, Andrew, additional, Medina Torres, Edgar Alejandro, additional, Scheffler Mendoza, Selma Cecilia, additional, Herrera Sanchez, Diana Andrea, additional, Lopez-Herrera, Gabriela, additional, Svyryd, Yevgeniya, additional, Mutchinick, Osvaldo M., additional, Gamazon, Eric, additional, Rathmell, Jeffrey C, additional, Itan, Yuval, additional, Markle, Janet, additional, O'Farrill Romanillos, Patricia, additional, Lugo-Reyes, Saul Oswaldo, additional, and Martinez-Barricarte, Ruben, additional

Published
2024
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19. Table S2 from Lactate Utilization Enables Metabolic Escape to Confer Resistance to BET Inhibition in Acute Myeloid Leukemia

Author

Monteith, Andrew J., primary, Ramsey, Haley E., primary, Silver, Alexander J., primary, Brown, Donovan, primary, Greenwood, Dalton, primary, Smith, Brianna N., primary, Wise, Ashley D., primary, Liu, Juan, primary, Olmstead, Sarah D., primary, Watke, Jackson, primary, Arrate, Maria P., primary, Gorska, Agnieszka E., primary, Fuller, Londa, primary, Locasale, Jason W., primary, Stubbs, Matthew C., primary, Rathmell, Jeffrey C., primary, and Savona, Michael R., primary

Published
2024
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20. Figure S4 from Lactate Utilization Enables Metabolic Escape to Confer Resistance to BET Inhibition in Acute Myeloid Leukemia

Author

Monteith, Andrew J., primary, Ramsey, Haley E., primary, Silver, Alexander J., primary, Brown, Donovan, primary, Greenwood, Dalton, primary, Smith, Brianna N., primary, Wise, Ashley D., primary, Liu, Juan, primary, Olmstead, Sarah D., primary, Watke, Jackson, primary, Arrate, Maria P., primary, Gorska, Agnieszka E., primary, Fuller, Londa, primary, Locasale, Jason W., primary, Stubbs, Matthew C., primary, Rathmell, Jeffrey C., primary, and Savona, Michael R., primary

Published
2024
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21. Data from Lactate Utilization Enables Metabolic Escape to Confer Resistance to BET Inhibition in Acute Myeloid Leukemia

Author

Monteith, Andrew J., primary, Ramsey, Haley E., primary, Silver, Alexander J., primary, Brown, Donovan, primary, Greenwood, Dalton, primary, Smith, Brianna N., primary, Wise, Ashley D., primary, Liu, Juan, primary, Olmstead, Sarah D., primary, Watke, Jackson, primary, Arrate, Maria P., primary, Gorska, Agnieszka E., primary, Fuller, Londa, primary, Locasale, Jason W., primary, Stubbs, Matthew C., primary, Rathmell, Jeffrey C., primary, and Savona, Michael R., primary

Published
2024
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25. Single-cell profiling of the antigen-specific response to BNT162b2 SARS-CoV-2 RNA vaccine

Author

Kramer, Kevin J., Wilfong, Erin M., Voss, Kelsey, Barone, Sierra M., Shiakolas, Andrea R., Raju, Nagarajan, Roe, Caroline E., Suryadevara, Naveenchandra, Walker, Lauren M., Wall, Steven C., Paulo, Ariana, Schaefer, Samuel, Dahunsi, Debolanle, Westlake, Camille S., Crowe, Jr, James E., Carnahan, Robert H., Rathmell, Jeffrey C., Bonami, Rachel H., Georgiev, Ivelin S., and Irish, Jonathan M.

Published
2022
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26. Single cell analysis of cribriform prostate cancer reveals cell intrinsic and tumor microenvironmental pathways of aggressive disease

Author

Wong, Hong Yuen, Sheng, Quanhu, Hesterberg, Amanda B., Croessmann, Sarah, Rios, Brenda L., Giri, Khem, Jackson, Jorgen, Miranda, Adam X., Watkins, Evan, Schaffer, Kerry R., Donahue, Meredith, Winkler, Elizabeth, Penson, David F., Smith, Joseph A., Herrell, S. Duke, Luckenbaugh, Amy N., Barocas, Daniel A., Kim, Young J., Graves, Diana, Giannico, Giovanna A., Rathmell, Jeffrey C., Park, Ben H., Gordetsky, Jennifer B., and Hurley, Paula J.

Published
2022
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28. Neutrophil trafficking to the site of infection requires Cpt1a-dependent fatty acid β-oxidation

Author

Pham, Ly, Komalavilas, Padmini, Eddie, Alex M., Thayer, Timothy E., Greenwood, Dalton L., Liu, Ken H., Weinberg, Jaclyn, Patterson, Andrew, Fessel, Joshua P., Boyd, Kelli L., Schafer, Jenny C., Kuck, Jamie L., Shaver, Aaron C., Flaherty, David K., Matlock, Brittany K., Wijers, Christiaan D. M., Serezani, C. Henrique, Jones, Dean P., Brittain, Evan L., Rathmell, Jeffrey C., and Noto, Michael J.

Published
2022
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31. Functional overlap of inborn errors of immunity and metabolism genes defines T cell metabolic vulnerabilities.

Author

Patterson, Andrew R., Needle, Gabriel A., Sugiura, Ayaka, Jennings, Erin Q., Chi, Channing, Steiner, KayLee K., Fisher, Emilie L., Robertson, Gabriella L., Bodnya, Caroline, Markle, Janet G., Sheldon, Ryan D., Jones, Russell G., Gama, Vivian, and Rathmell, Jeffrey C.

Subjects
HUMAN biology, INBORN errors of metabolism, T cell differentiation, T cells, URIDINE diphosphate
Abstract

Inborn errors of metabolism (IEMs) and immunity (IEIs) are Mendelian diseases in which complex phenotypes and patient rarity have limited clinical understanding. Whereas few genes have been annotated as contributing to both IEMs and IEIs, immunometabolic demands suggested greater functional overlap. Here, CRISPR screens tested IEM genes for immunologic roles and IEI genes for metabolic effects and found considerable previously unappreciated crossover. Analysis of IEMs showed that N-linked glycosylation and the hexosamine pathway enzyme Gfpt1 are critical for T cell expansion and function. Further, T helper (TH1) cells synthesized uridine diphosphate N-acetylglucosamine more rapidly and were more impaired by Gfpt1 deficiency than TH17 cells. Screening IEI genes found that Bcl11b promotes the CD4 T cell mitochondrial activity and Mcl1 expression necessary to prevent metabolic stress. Thus, a high degree of functional overlap exists between IEM and IEI genes, and immunometabolic mechanisms may underlie a previously underappreciated intersection of these disorders. Editor's summary: Inborn errors of metabolism (IEMs) and immunity (IEIs) are two groups of monogenic disorders whose study has offered insights into fundamental human biology. Patterson et al. used CRISPR screens of mouse CD4 T cells disrupting known IEM and IEI genes to test potential overlapping immunometabolic regulators of T cell function. This approach revealed hundreds of previously unappreciated players, including N-linked glycosylation and the de novo hexosamine synthesis enzyme Gfpt1, which were critical for T cell expansion and function. Moreover, Bcl11b, a player in thymic T cell differentiation, promoted mitochondrial activity and prevented metabolic stress in CD4 T cells. —Seth Thomas Scanlon [ABSTRACT FROM AUTHOR]

Published
2024
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34. Metabolite profiling of human renal cell carcinoma reveals tissue-origin dominance in nutrient availability

Author

Abbott, Keene L., primary, Ali, Ahmed, additional, Reinfeld, Bradley I., additional, Deik, Amy, additional, Subudhi, Sonu, additional, Landis, Madelyn D., additional, Hongo, Rachel A., additional, Young, Kirsten L., additional, Kunchok, Tenzin, additional, Nabel, Christopher S., additional, Crowder, Kayla D., additional, Kent, Johnathan R., additional, Madariaga, Maria Lucia L., additional, Jain, Rakesh K., additional, Beckermann, Kathryn E., additional, Lewis, Caroline A., additional, Clish, Clary B., additional, Muir, Alexander, additional, Rathmell, W. Kimryn, additional, Rathmell, Jeffrey C., additional, and Heiden, Matthew G. Vander, additional

Published
2024
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35. Scalable single-cell pooled CRISPR screens with conventional knockout vector libraries

Author

Islam, Mirazul, primary, Yang, Yilin, additional, Simmons, Alan J., additional, Xu, Yanwen, additional, Fisher, Emilie L., additional, Deng, Wentao, additional, Grieb, Brian C, additional, Molina, Paola, additional, de Caestecker, Christian, additional, Ramirez-Solano, Marisol A., additional, Liu, Qi, additional, Tansey, William P., additional, Macara, Ian G., additional, Rathmell, Jeffrey C., additional, Coffey, Robert J., additional, and Lau, Ken S., additional

Published
2024
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36. Cell-programmed nutrient partitioning in the tumour microenvironment

Author

Reinfeld, Bradley I., Madden, Matthew Z., Wolf, Melissa M., Chytil, Anna, Bader, Jackie E., Patterson, Andrew R., Sugiura, Ayaka, Cohen, Allison S., Ali, Ahmed, Do, Brian T., Muir, Alexander, Lewis, Caroline A., Hongo, Rachel A., Young, Kirsten L., Brown, Rachel E., Todd, Vera M., Huffstater, Tessa, Abraham, Abin, O’Neil, Richard T., Wilson, Matthew H., Xin, Fuxue, Tantawy, M. Noor, Merryman, W. David, Johnson, Rachelle W., Williams, Christopher S., Mason, Emily F., Mason, Frank M., Beckermann, Katherine E., Vander Heiden, Matthew G., Manning, H. Charles, Rathmell, Jeffrey C., and Rathmell, W. Kimryn

Published
2021
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37. Metabolite profiling of human renal cell carcinoma reveals tissue-origin dominance in nutrient availability

Author

Abbott, Keene L, primary, Ali, Ahmed, additional, Reinfeld, Bradley I, additional, Deik, Amy Anderson I, additional, Subudhi, Sonu, additional, Landis, Madelyn D, additional, Hongo, Rachel A, additional, Young, Kirsten L, additional, Kunchok, Tenzin, additional, Nabel, Christopher S, additional, Crowder, Kayla D, additional, Kent, Johnathan R, additional, Madariaga, Maria Lucia L, additional, Jain, Rakesh K, additional, Beckermann, Kathryn E, additional, Lewis, Caroline A, additional, Clish, Clary B., additional, Muir, Alexander, additional, Rathmell, W. Kimryn, additional, Rathmell, Jeffrey C, additional, and Vander Heiden, Matthew G, additional

Published
2023
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38. Protein kinase C delta regulates mononuclear phagocytes and hinders response to immunotherapy in cancer

Author

Chaib, Mehdi, primary, Holt, Jeremiah R., additional, Fisher, Emilie L., additional, Sipe, Laura M., additional, Bohm, Margaret S., additional, Joseph, Sydney C., additional, Simmons, Boston W., additional, Eugin Simon, Samson, additional, Yarbro, Johnathan R., additional, Tanveer, Ubaid, additional, Halle, Jessica L., additional, Carson, James A., additional, Hollingsworth, T.J., additional, Wei, QingQing, additional, Rathmell, Jeffrey C., additional, Thomas, Paul G., additional, Hayes, D. Neil, additional, and Makowski, Liza, additional

Published
2023
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39. Temporal recording of mammalian development and precancer

Author

Islam, Mirazul, primary, Yang, Yilin, additional, Simmons, Alan J., additional, Shah, Vishal M., additional, Pavan, Musale Krushna, additional, Xu, Yanwen, additional, Tasneem, Naila, additional, Chen, Zhengyi, additional, Trinh, Linh T., additional, Molina, Paola, additional, Ramirez-Solano, Marisol A., additional, Sadien, Iannish, additional, Dou, Jinzhuang, additional, Chen, Ken, additional, Magnuson, Mark A., additional, Rathmell, Jeffrey C., additional, Macara, Ian G., additional, Winton, Douglas, additional, Liu, Qi, additional, Zafar, Hamim, additional, Kalhor, Reza, additional, Church, George M., additional, Shrubsole, Martha J., additional, Coffey, Robert J., additional, and Lau, Ken S., additional

Published
2023
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41. Control of PI(3) kinase in Treg cells maintains homeostasis and lineage stability

Author

Huynh, Alexandria, DuPage, Michel, Priyadharshini, Bhavana, Sage, Peter T, Quiros, Jason, Borges, Christopher M, Townamchai, Natavudh, Gerriets, Valerie A, Rathmell, Jeffrey C, Sharpe, Arlene H, Bluestone, Jeffrey A, and Turka, Laurence A

Subjects
Biochemistry and Cell Biology, Biological Sciences, Generic health relevance, Animals, Cell Lineage, Enzyme-Linked Immunosorbent Assay, Flow Cytometry, Gene Deletion, Homeostasis, Mice, PTEN Phosphohydrolase, Phosphatidylinositol 3-Kinases, Signal Transduction, T-Lymphocytes, Regulatory, Immunology, Biochemistry and cell biology
Abstract

Foxp3(+) regulatory T cells (Treg cells) are required for immunological homeostasis. One notable distinction between conventional T cells (Tconv cells) and Treg cells is differences in the activity of phosphatidylinositol-3-OH kinase (PI(3)K); only Tconv cells downregulate PTEN, the main negative regulator of PI(3)K, upon activation. Here we found that control of PI(3)K in Treg cells was essential for lineage homeostasis and stability. Mice lacking Pten in Treg cells developed an autoimmune-lymphoproliferative disease characterized by excessive T helper type 1 (TH1) responses and B cell activation. Diminished control of PI(3)K activity in Treg cells led to reduced expression of the interleukin-2 (IL-2) receptor α subunit CD25, accumulation of Foxp3(+)CD25(-) cells and, ultimately, loss of expression of the transcription factor Foxp3 in these cells. Collectively, our data demonstrate that control of PI(3)K signaling by PTEN in Treg cells is critical for maintaining their homeostasis, function and stability.

Published
2015

44. Tissue-Specific Dependence of Th1 Cells on the Amino Acid Transporter SLC38A1 in Inflammation

Author

Sugiura, Ayaka, primary, Beier, Katherine L., additional, Chi, Channing, additional, Heintzman, Darren R., additional, Ye, Xiang, additional, Wolf, Melissa M., additional, Patterson, Andrew R., additional, Cephus, Jacqueline-Yvonne, additional, Hong, Hanna S., additional, Lyssiotis, Costas A., additional, Newcomb, Dawn C., additional, and Rathmell, Jeffrey C., additional

Published
2023
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48. MYC and MCL1 Cooperatively Promote Chemotherapy-Resistant Breast Cancer Stem Cells via Regulation of Mitochondrial Oxidative Phosphorylation

Author

Lee, Kyung-min, Giltnane, Jennifer M., Balko, Justin M., Schwarz, Luis J., Guerrero-Zotano, Angel L., Hutchinson, Katherine E., Nixon, Mellissa J., Estrada, Mónica V., Sánchez, Violeta, Sanders, Melinda E., Lee, Taekyu, Gómez, Henry, Lluch, Ana, Pérez-Fidalgo, J. Alejandro, Wolf, Melissa Magdalene, Andrejeva, Gabriela, Rathmell, Jeffrey C., Fesik, Stephen W., and Arteaga, Carlos L.

Published
2017
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50. STING-activating nanoparticles normalize the vascular-immune interface to potentiate cancer immunotherapy

Author

Wang-Bishop, Lihong, primary, Kimmel, Blaise R., additional, Ngwa, Verra M., additional, Madden, Matthew Z., additional, Baljon, Jessalyn J., additional, Florian, David C., additional, Hanna, Ann, additional, Pastora, Lucinda E., additional, Sheehy, Taylor L., additional, Kwiatkowski, Alexander J., additional, Wehbe, Mohamed, additional, Wen, Xiaona, additional, Becker, Kyle W., additional, Garland, Kyle M., additional, Schulman, Jacob A., additional, Shae, Daniel, additional, Edwards, Deanna, additional, Wolf, Melissa M., additional, Delapp, Rossane, additional, Christov, Plamen P., additional, Beckermann, Kathryn E., additional, Balko, Justin M., additional, Rathmell, W. Kimryn, additional, Rathmell, Jeffrey C., additional, Chen, Jin, additional, and Wilson, John T., additional

Published
2023
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