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Article ; Online: Metabolic but not transcriptional regulation by PKM2 is important for natural killer cell responses.

Walls, Jessica F / Subleski, Jeff J / Palmieri, Erika M / Gonzalez-Cotto, Marieli / Gardiner, Clair M / McVicar, Daniel W / Finlay, David K

eLife

2020 Volume 9

Abstract: Natural Killer (NK) cells have an important role in immune responses to viruses and tumours. Integrating changes in signal transduction pathways and cellular metabolism is essential for effective NK cells responses. The glycolytic enzyme Pyruvate Kinase ... ...

Abstract	Natural Killer (NK) cells have an important role in immune responses to viruses and tumours. Integrating changes in signal transduction pathways and cellular metabolism is essential for effective NK cells responses. The glycolytic enzyme Pyruvate Kinase Muscle 2 (PKM2) has described roles in regulating glycolytic flux and signal transduction, particularly gene transcription. While PKM2 expression is robustly induced in activated NK cells, mice lacking PKM2 in NK cells showed no defect in NK cell metabolism, transcription or antiviral responses to MCMV infection. NK cell metabolism was maintained due to compensatory PKM1 expression in PKM2-null NK cells. To further investigate the role of PKM2, we used TEPP-46, which increases PKM2 catalytic activity while inhibiting any PKM2 signalling functions. NK cells activated with TEPP-46 had reduced effector function due to TEPP-46-induced increases in oxidative stress. Overall, PKM2-regulated glycolytic metabolism and redox status, not transcriptional control, facilitate optimal NK cells responses.
MeSH term(s)	Animals ; Cells, Cultured ; Gene Expression Regulation/drug effects ; Gene Expression Regulation/genetics ; Glycolysis/drug effects ; Glycolysis/genetics ; Killer Cells, Natural/metabolism ; Mice ; Oxidative Stress ; Pyridazines/pharmacology ; Pyrroles/pharmacology ; Pyruvate Kinase/antagonists & inhibitors ; Pyruvate Kinase/genetics ; Pyruvate Kinase/metabolism ; Signal Transduction
Chemical Substances	ML-265 ; Pyridazines ; Pyrroles ; Pkm protein, mouse (EC 2.7.1.40) ; Pyruvate Kinase (EC 2.7.1.40)
Language	English
Publishing date	2020-08-19
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.59166
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Editorial: NKT cells: to suppress or not to suppress, that is the question.

Subleski, Jeff J / Ortaldo, John R

Journal of leukocyte biology

2009 Volume 86, Issue 4, Page(s) 751–752

MeSH term(s)	Cell Differentiation/drug effects ; Cell Differentiation/immunology ; Cells, Cultured ; Coculture Techniques ; Dendritic Cells/cytology ; Dendritic Cells/immunology ; Granulocyte-Macrophage Colony-Stimulating Factor/pharmacology ; Humans ; Immune Tolerance/drug effects ; Immune Tolerance/immunology ; Interferon-gamma/immunology ; Interleukin-10/immunology ; Interleukin-12/immunology ; Interleukin-4/pharmacology ; Monocytes/cytology ; Monocytes/immunology ; Natural Killer T-Cells/cytology ; Natural Killer T-Cells/immunology ; Th1 Cells/cytology ; Th1 Cells/immunology
Chemical Substances	IL10 protein, human ; IL4 protein, human ; Interleukin-10 (130068-27-8) ; Interleukin-12 (187348-17-0) ; Interleukin-4 (207137-56-2) ; Interferon-gamma (82115-62-6) ; Granulocyte-Macrophage Colony-Stimulating Factor (83869-56-1)
Language	English
Publishing date	2009-10-01
Publishing country	United States
Document type	Comment ; Editorial
ZDB-ID	605722-6
ISSN	1938-3673 ; 0741-5400
ISSN (online)	1938-3673
ISSN	0741-5400
DOI	10.1189/jlb.0309118
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Article ; Online: Metabolic but not transcriptional regulation by PKM2 is important for natural killer cell responses

Jessica F Walls / Jeff J Subleski / Erika M Palmieri / Marieli Gonzalez-Cotto / Clair M Gardiner / Daniel W McVicar / David K Finlay

eLife, Vol

2020 Volume 9

Abstract	Natural Killer (NK) cells have an important role in immune responses to viruses and tumours. Integrating changes in signal transduction pathways and cellular metabolism is essential for effective NK cells responses. The glycolytic enzyme Pyruvate Kinase Muscle 2 (PKM2) has described roles in regulating glycolytic flux and signal transduction, particularly gene transcription. While PKM2 expression is robustly induced in activated NK cells, mice lacking PKM2 in NK cells showed no defect in NK cell metabolism, transcription or antiviral responses to MCMV infection. NK cell metabolism was maintained due to compensatory PKM1 expression in PKM2-null NK cells. To further investigate the role of PKM2, we used TEPP-46, which increases PKM2 catalytic activity while inhibiting any PKM2 signalling functions. NK cells activated with TEPP-46 had reduced effector function due to TEPP-46-induced increases in oxidative stress. Overall, PKM2-regulated glycolytic metabolism and redox status, not transcriptional control, facilitate optimal NK cells responses.
Keywords	metabolism ; immunology ; nk cells ; Medicine ; R ; Science ; Q ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2020-08-01T00:00:00Z
Publisher	eLife Sciences Publications Ltd
Document type	Article ; Online
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Article ; Online: Application of tissue-specific NK and NKT cell activity for tumor immunotherapy.

Subleski, Jeff J / Wiltrout, Robert H / Weiss, Jonathan M

Journal of autoimmunity

2009 Volume 33, Issue 3-4, Page(s) 275–281

Abstract: Natural killer (NK) and NKT cells are a first line of defense against pathogens and transformed cells. However, dysregulation of their function can lead to autoimmune disease. A better understanding of the mechanisms controlling NK and NKT effector ... ...

Abstract	Natural killer (NK) and NKT cells are a first line of defense against pathogens and transformed cells. However, dysregulation of their function can lead to autoimmune disease. A better understanding of the mechanisms controlling NK and NKT effector function should lead to the development of improved strategies for the treatment of many diseases. The site in which NK and NKT cells reside should be taken into account, because accumulating evidence suggests that the tissue microenvironment strongly influences their function. In this regard, the liver represents a unique immunologic organ in which the balance between the need for tolerance and the ability to respond rapidly to pathogens and tissue injury is tightly regulated. NK cells in the liver have augmented cytolytic activity as compared to other organs, which is consistent with a role for liver-associated NK cells in being critical effector cells for inhibiting tumor metastasis in the liver. Several studies also suggest that hepatic NKT cells have different functions than those in other organs. Whereas splenic and thymic NKT cells have been shown to suppress diabetes development, facilitate the induction of systemic tolerance and are regulated by IL-4 and other Th2 cytokines, certain subsets of NKT cells in the liver are important sources of Th1 cytokines such as Interferon gamma, and are the primary mediators of anti-tumor responses. The unique properties and roles as critical effector cells make NK and NKT cells within the liver microenvironment attractive targets of immunotherapeutic approaches that have the goal of controlling tumor metastasis in the liver.
MeSH term(s)	Animals ; Cytokines/immunology ; Cytotoxicity, Immunologic ; Humans ; Immunologic Surveillance ; Immunotherapy/methods ; Killer Cells, Natural/immunology ; Liver/immunology ; Liver/pathology ; Liver Neoplasms/secondary ; Liver Neoplasms/therapy ; Natural Killer T-Cells/immunology ; Neoplasm Metastasis
Chemical Substances	Cytokines
Language	English
Publishing date	2009-08-13
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	639452-8
ISSN	1095-9157 ; 0896-8411
ISSN (online)	1095-9157
ISSN	0896-8411
DOI	10.1016/j.jaut.2009.07.010
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Article ; Online: The split personality of NKT cells in malignancy, autoimmune and allergic disorders.

Subleski, Jeff J / Jiang, Qun / Weiss, Jonathan M / Wiltrout, Robert H

Immunotherapy

2011 Volume 3, Issue 10, Page(s) 1167–1184

Abstract: NKT cells are a heterogeneous subset of specialized, self-reactive T cells, with innate and adaptive immune properties, which allow them to bridge innate and adaptive immunity and profoundly influence autoimmune and malignant disease outcomes. NKT cells ... ...

Abstract	NKT cells are a heterogeneous subset of specialized, self-reactive T cells, with innate and adaptive immune properties, which allow them to bridge innate and adaptive immunity and profoundly influence autoimmune and malignant disease outcomes. NKT cells mediate these activities through their ability to rapidly express pro- and anti-inflammatory cytokines that influence the type and magnitude of the immune response. Not only do NKT cells regulate the functions of other cell types, but experimental evidence has found NKT cell subsets can modulate the functions of other NKT subsets. Depending on underlying mechanisms, NKT cells can inhibit or exacerbate autoimmunity and malignancy, making them potential targets for disease intervention. NKT cells can respond to foreign and endogenous antigenic glycolipid signals that are expressed during pathogenic invasion or ongoing inflammation, respectively, allowing them to rapidly react to and influence a broad array of diseases. In this article we review the unique development and activation pathways of NKT cells and focus on how these attributes augment or exacerbate autoimmune disorders and malignancy. We also examine the growing evidence that NKT cells are involved in liver inflammatory conditions that can contribute to the development of malignancy.
MeSH term(s)	Animals ; Autoantigens/immunology ; Autoimmune Diseases/immunology ; Autoimmune Diseases/therapy ; Cell Transformation, Neoplastic/immunology ; Cytokines/immunology ; Disease Models, Animal ; Glycolipids/immunology ; Humans ; Hypersensitivity/immunology ; Hypersensitivity/therapy ; Immunity, Cellular ; Immunotherapy, Adoptive ; Inflammation ; Mice ; Natural Killer T-Cells/immunology ; Neoplasms/immunology ; Neoplasms/pathology ; Neoplasms/therapy
Chemical Substances	Autoantigens ; Cytokines ; Glycolipids
Language	English
Publishing date	2011-10-13
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Review
ISSN	1750-7448
ISSN (online)	1750-7448
DOI	10.2217/imt.11.117
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Tumour-elicited neutrophils engage mitochondrial metabolism to circumvent nutrient limitations and maintain immune suppression.

Rice, Christopher M / Davies, Luke C / Subleski, Jeff J / Maio, Nunziata / Gonzalez-Cotto, Marieli / Andrews, Caroline / Patel, Nimit L / Palmieri, Erika M / Weiss, Jonathan M / Lee, Jung-Min / Annunziata, Christina M / Rouault, Tracey A / Durum, Scott K / McVicar, Daniel W

Nature communications

2018 Volume 9, Issue 1, Page(s) 5099

Abstract: Neutrophils are a vital component of immune protection, yet in cancer they may promote tumour progression, partly by generating reactive oxygen species (ROS) that disrupts lymphocyte functions. Metabolically, neutrophils are often discounted as purely ... ...

Abstract	Neutrophils are a vital component of immune protection, yet in cancer they may promote tumour progression, partly by generating reactive oxygen species (ROS) that disrupts lymphocyte functions. Metabolically, neutrophils are often discounted as purely glycolytic. Here we show that immature, c-Kit
MeSH term(s)	Animals ; CRISPR-Cas Systems ; Cell Line, Tumor ; Cells, Cultured ; Flow Cytometry ; Immunoblotting ; Immunohistochemistry ; Mice ; Mice, Knockout ; Microscopy, Confocal ; Mitochondria/metabolism ; Neutrophils/metabolism ; Neutrophils/physiology ; Oxidation-Reduction ; Oxidative Phosphorylation ; Oxidative Stress ; Reactive Oxygen Species/metabolism ; Signal Transduction/physiology
Chemical Substances	Reactive Oxygen Species
Language	English
Publishing date	2018-11-30
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-018-07505-2
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Article ; Online: Immunotherapy of cancer by IL-12-based cytokine combinations.

Weiss, Jonathan M / Subleski, Jeff J / Wigginton, Jon M / Wiltrout, Robert H

Expert opinion on biological therapy

2007 Volume 7, Issue 11, Page(s) 1705–1721

Abstract: Cancer is a multi-faceted disease comprising complex interactions between neoplastic and normal cells. Over the past decade, there has been considerable progress in defining the molecular, cellular and environmental contributions to the pathophysiology ... ...

Abstract	Cancer is a multi-faceted disease comprising complex interactions between neoplastic and normal cells. Over the past decade, there has been considerable progress in defining the molecular, cellular and environmental contributions to the pathophysiology of tumor development. Despite these advances, the conventional treatment of patients still generally involves surgery, radiotherapy and/or chemotherapy, and the clinical outcome for many of these efforts remains unsatisfactory. Recent studies have highlighted the feasibility of using immunotherapeutic approaches that seek to enhance host immune responses to developing tumors. These strategies include immunomodulatory cytokines, with TNF-alpha, type I or type II IFNs, IL-2, IL-12, IL-15 and IL-18 being among the most potent inducers of anti-tumor activity in a variety of preclinical studies. More recently, some exciting new cytokines have been characterized, such as IL-21, IL-23, IL-27 and their immunomodulatory and antitumor effects in vitro and in vivo suggest that they may have considerable promise for future immunotherapy protocols. The promise of cytokine therapy does indeed derive from the identification of these novel cytokines but even more fundamentally, the field is greatly benefiting from the ever-expanding amount of preclinical data that convincingly demonstrate synergistic and/or novel biologic effects, which may be achieved through the use of several combinations of cytokines with complementary immune-stimulating capabilities. One cytokine in particular, IL-12, holds considerable promise by virtue of the fact that it plays a central role in regulating both innate and adaptive immune responses, can by itself induce potent anticancer effects, and synergizes with several other cytokines for increased immunoregulatory and antitumor activities. This review discusses the antitumor activity of IL-12, with a special emphasis on its ability to synergize with other cytokines for enhancement of immune effector cell populations and regulation of host-tumor cell interactions and the overall tumor microenvironment.
MeSH term(s)	Humans ; Immunity, Cellular ; Immunotherapy ; Interleukin-12/therapeutic use ; Neoplasms/therapy
Chemical Substances	Interleukin-12 (187348-17-0)
Language	English
Publishing date	2007-10-26
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2052501-1
ISSN	1744-7682 ; 1471-2598
ISSN (online)	1744-7682
ISSN	1471-2598
DOI	10.1517/14712598.7.11.1705
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Zs.A 6094: Show issues

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Article ; Online: Tumour-elicited neutrophils engage mitochondrial metabolism to circumvent nutrient limitations and maintain immune suppression

Christopher M. Rice / Luke C. Davies / Jeff J. Subleski / Nunziata Maio / Marieli Gonzalez-Cotto / Caroline Andrews / Nimit L. Patel / Erika M. Palmieri / Jonathan M. Weiss / Jung-Min Lee / Christina M. Annunziata / Tracey A. Rouault / Scott K. Durum / Daniel W. McVicar

Nature Communications, Vol 9, Iss 1, Pp 1-

2018 Volume 13

Abstract: Neutrophils normally fulfil their metabolic demands by glycolysis and have limited mitochondrial activity. Here the authors show that tumours promote neutrophils adapted to oxidative mitochondria metabolism that function in the glucose-restrained tumour ... ...

Abstract	Neutrophils normally fulfil their metabolic demands by glycolysis and have limited mitochondrial activity. Here the authors show that tumours promote neutrophils adapted to oxidative mitochondria metabolism that function in the glucose-restrained tumour microenvironment to promote tumour growth by maintaining local immune suppression.
Keywords	Science ; Q
Language	English
Publishing date	2018-11-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Tumour-elicited neutrophils engage mitochondrial metabolism to circumvent nutrient limitations and maintain immune suppression

Nature Communications, Vol 9, Iss 1, Pp 1-

2018 Volume 13

Abstract	Neutrophils normally fulfil their metabolic demands by glycolysis and have limited mitochondrial activity. Here the authors show that tumours promote neutrophils adapted to oxidative mitochondria metabolism that function in the glucose-restrained tumour microenvironment to promote tumour growth by maintaining local immune suppression.
Keywords	Science ; Q
Language	English
Publishing date	2018-11-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Serum-based tracking of de novo initiated liver cancer progression reveals early immunoregulation and response to therapy.

Subleski, Jeff J / Scarzello, Anthony J / Alvord, W Gregory / Jiang, Qun / Stauffer, Jimmy K / Kronfli, Anthony / Saleh, Bahara / Back, Timothy / Weiss, Jonathan M / Wiltrout, Robert H

Journal of hepatology

2015 Volume 63, Issue 5, Page(s) 1181–1189

Abstract: Background & aims: Liver inflammatory diseases associated with cancer promoting somatic oncogene mutations are increasing in frequency. Preclinical cancer models that allow for the study of early tumor progression are often protracted, which limits the ... ...

Abstract	Background & aims: Liver inflammatory diseases associated with cancer promoting somatic oncogene mutations are increasing in frequency. Preclinical cancer models that allow for the study of early tumor progression are often protracted, which limits the experimental study parameters due to time and expense. Here we report a robust inexpensive approach using Sleeping Beauty transposition (SBT) delivery of oncogenes along with Gaussia Luciferase expression vector GLuc, to assess de novo liver tumor progression, as well as the detection of innate immune responses or responses induced by therapeutic intervention. Methods: Tracking de novo liver tumor progression with GLuc was demonstrated in models of hepatocellular carcinoma (HCC) or adenoma (HCA) initiated by hydrodynamic delivery of SBT oncogenes. Results: Rising serum luciferase levels correlated directly with increasing liver tumor burden and eventual morbidity. Early detection of hepatocyte apoptosis from mice with MET+CAT transfected hepatocytes was associated with a transient delay in HCC growth mediated by a CD8(+) T-cell response against transformed hepatocytes. Furthermore, mice that lack B cells or macrophages had an increase in TUNEL(+) hepatocytes following liver MET transfection demonstrating that these cells provide protection from MET-induced hepatocyte apoptosis. Treatment with IL-18+IL-12 of mice displaying established HCC decreased tumor burden which was associated with decreased levels of serum luciferase. Conclusions: Hydrodynamic delivery of the SBT vector GLuc to hepatocytes serves as a simple blood-based approach for real-time tracking of pathologically distinct types of liver cancer. This revealed tumor-induced immunologic responses and was beneficial in monitoring the efficacy of therapeutic interventions.
MeSH term(s)	Adenoma, Liver Cell/drug therapy ; Adenoma, Liver Cell/immunology ; Adenoma, Liver Cell/pathology ; Animals ; Apoptosis ; CD8-Positive T-Lymphocytes/immunology ; Carcinoma, Hepatocellular/drug therapy ; Carcinoma, Hepatocellular/immunology ; Carcinoma, Hepatocellular/pathology ; Disease Progression ; Hepatocytes/pathology ; Immunity, Cellular ; Immunohistochemistry ; In Situ Nick-End Labeling ; Interleukin-12/therapeutic use ; Interleukin-18/therapeutic use ; Liver Neoplasms/drug therapy ; Liver Neoplasms/immunology ; Liver Neoplasms/pathology ; Liver Neoplasms, Experimental/drug therapy ; Liver Neoplasms, Experimental/immunology ; Liver Neoplasms, Experimental/pathology ; Luciferases/blood ; Magnetic Resonance Imaging ; Mice ; Mice, Inbred C57BL ; Recombinant Proteins/therapeutic use ; Signal Transduction
Chemical Substances	Interleukin-18 ; Recombinant Proteins ; Interleukin-12 (187348-17-0) ; Luciferases (EC 1.13.12.-)
Language	English
Publishing date	2015-07-02
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	605953-3
ISSN	1600-0641 ; 0168-8278
ISSN (online)	1600-0641
ISSN	0168-8278
DOI	10.1016/j.jhep.2015.06.021
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