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Article ; Online: How the Unfolded Protein Response Is a Boon for Tumors and a Bane for the Immune System.

Raines, Lydia N / Huang, Stanley Ching-Cheng

ImmunoHorizons

2023 Volume 7, Issue 4, Page(s) 256–264

Abstract: The correct folding of proteins is essential for appropriate cell function and is tightly regulated within the endoplasmic reticulum (ER). Environmental challenges and cellular conditions disrupt ER homeostasis and induce ER stress, which adversely ... ...

Abstract	The correct folding of proteins is essential for appropriate cell function and is tightly regulated within the endoplasmic reticulum (ER). Environmental challenges and cellular conditions disrupt ER homeostasis and induce ER stress, which adversely affect protein folding and activate the unfolded protein response (UPR). It is now becoming recognized that cancer cells can overcome survival challenges posed within the tumor microenvironment by activating the UPR. Furthermore, the UPR has also been found to impose detrimental effects on immune cells by inducing immunoinhibitory activity in both tumor-infiltrating innate and adaptive immune cells. This suggests that these signaling axes may be important therapeutic targets, resulting in multifaceted approaches to eradicating tumor cells. In this mini-review, we discuss the role of the UPR in driving tumor progression and modulating the immune system's ability to target cancer cells. Additionally, we highlight some of the key unanswered questions that may steer future UPR research.
MeSH term(s)	Humans ; Unfolded Protein Response ; Endoplasmic Reticulum Stress ; Neoplasms/pathology ; Endoplasmic Reticulum/metabolism ; Endoplasmic Reticulum/pathology ; Immune System ; Tumor Microenvironment
Language	English
Publishing date	2023-04-17
Publishing country	United States
Document type	Review ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2573-7732
ISSN (online)	2573-7732
DOI	10.4049/immunohorizons.2200064
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Article ; Online: Control of immune cell function by the unfolded protein response.

Di Conza, Giusy / Ho, Ping-Chih / Cubillos-Ruiz, Juan R / Huang, Stanley Ching-Cheng

Nature reviews. Immunology

2023 Volume 23, Issue 9, Page(s) 546–562

Abstract: Initiating and maintaining optimal immune responses requires high levels of protein synthesis, folding, modification and trafficking in leukocytes, which are processes orchestrated by the endoplasmic reticulum. Importantly, diverse extracellular and ... ...

Abstract	Initiating and maintaining optimal immune responses requires high levels of protein synthesis, folding, modification and trafficking in leukocytes, which are processes orchestrated by the endoplasmic reticulum. Importantly, diverse extracellular and intracellular conditions can compromise the protein-handling capacity of this organelle, inducing a state of 'endoplasmic reticulum stress' that activates the unfolded protein response (UPR). Emerging evidence shows that physiological or pathological activation of the UPR can have effects on immune cell survival, metabolism, function and fate. In this Review, we discuss the canonical role of the adaptive UPR in immune cells and how dysregulation of this pathway in leukocytes contributes to diverse pathologies such as cancer, autoimmunity and metabolic disorders. Furthermore, we provide an overview as to how pharmacological approaches that modulate the UPR could be harnessed to control or activate immune cell function in disease.
MeSH term(s)	Humans ; Unfolded Protein Response ; Endoplasmic Reticulum Stress ; Neoplasms/pathology ; Immunity ; Endoplasmic Reticulum/metabolism
Language	English
Publishing date	2023-02-08
Publishing country	England
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2062776-2
ISSN	1474-1741 ; 1474-1733
ISSN (online)	1474-1741
ISSN	1474-1733
DOI	10.1038/s41577-023-00838-0
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Zs.A 5565: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 34: Show issues

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Article ; Online: Breathe In, Breathe Out: Metabolic Regulation of Lung Macrophages in Host Defense Against Bacterial Infection.

Andrews, J Tucker / Voth, Daniel E / Huang, Stanley Ching-Cheng / Huang, Lu

Frontiers in cellular and infection microbiology

2022 Volume 12, Page(s) 934460

Abstract: Lung macrophages are substantially distinct from other tissue-resident macrophages. They act as frontier sentinels of the alveolar-blood interface and are constantly exposed to various pathogens. Additionally, they precisely regulate immune responses ... ...

Abstract	Lung macrophages are substantially distinct from other tissue-resident macrophages. They act as frontier sentinels of the alveolar-blood interface and are constantly exposed to various pathogens. Additionally, they precisely regulate immune responses under homeostatic and pathological conditions to curtail tissue damage while containing respiratory infections. As a highly heterogeneous population, the phenotypes and functions of lung macrophages with differing developmental ontogenies are linked to both intrinsic and extrinsic metabolic processes. Importantly, targeting these metabolic pathways greatly impacts macrophage functions, which in turn leads to different disease outcomes in the lung. In this review, we will discuss underlying metabolic regulation of lung macrophage subsets and how metabolic circuits, together with epigenetic modifications, dictate lung macrophage function during bacterial infection.
MeSH term(s)	Bacterial Infections/pathology ; Humans ; Immunity ; Lung/microbiology ; Macrophages ; Macrophages, Alveolar
Language	English
Publishing date	2022-07-08
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2619676-1
ISSN	2235-2988 ; 2235-2988
ISSN (online)	2235-2988
ISSN	2235-2988
DOI	10.3389/fcimb.2022.934460
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Article ; Online: Is glucose the scapegoat for tumor evasion?

Raines, Lydia N / Huang, Stanley Ching-Cheng

Cancer cell

2021 Volume 39, Issue 7, Page(s) 907–909

Abstract: Tumor cells undergo rapid aerobic glycolysis to fuel growth and proliferation. A recent finding in Nature reveals that tumor-infiltrating myeloid cells demonstrate greater capacity for glucose uptake than tumor cells and consume significant amounts ... ...

Abstract	Tumor cells undergo rapid aerobic glycolysis to fuel growth and proliferation. A recent finding in Nature reveals that tumor-infiltrating myeloid cells demonstrate greater capacity for glucose uptake than tumor cells and consume significant amounts within the tumor milieu. Unexpectedly, tumor cells account for the highest glutamine utilization in the tumor microenvironment.
MeSH term(s)	Glucose ; Glutamine/metabolism ; Glycolysis ; Humans ; Neoplasms ; Tumor Microenvironment
Chemical Substances	Glutamine (0RH81L854J) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2021-07-13
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	2078448-X
ISSN	1878-3686 ; 1535-6108
ISSN (online)	1878-3686
ISSN	1535-6108
DOI	10.1016/j.ccell.2021.06.006
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Zs.A 5650: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 104: Show issues

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Article: Molecular Chaperones: Molecular Assembly Line Brings Metabolism and Immunity in Shape.

Zhao, Haoxin / Raines, Lydia N / Huang, Stanley Ching-Cheng

Metabolites

2020 Volume 10, Issue 10

Abstract: Molecular chaperones are a set of conserved proteins that have evolved to assist the folding of many newly synthesized proteins by preventing their misfolding under conditions such as elevated temperatures, hypoxia, acidosis and nutrient deprivation. ... ...

Abstract	Molecular chaperones are a set of conserved proteins that have evolved to assist the folding of many newly synthesized proteins by preventing their misfolding under conditions such as elevated temperatures, hypoxia, acidosis and nutrient deprivation. Molecular chaperones belong to the heat shock protein (HSP) family. They have been identified as important participants in immune functions including antigen presentation, immunostimulation and immunomodulation, and play crucial roles in metabolic rewiring and epigenetic circuits. Growing evidence has accumulated to indicate that metabolic pathways and their metabolites influence the function of immune cells and can alter transcriptional activity through epigenetic modification of (de)methylation and (de)acetylation. However, whether molecular chaperones can regulate metabolic programs to influence immune activity is still largely unclear. In this review, we discuss the available data on the biological function of molecular chaperones to immune responses during inflammation, with a specific focus on the interplay between molecular chaperones and metabolic pathways that drive immune cell fate and function.
Language	English
Publishing date	2020-10-03
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2662251-8
ISSN	2218-1989
ISSN	2218-1989
DOI	10.3390/metabo10100394
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Article ; Online: Carbohydrate and Amino Acid Metabolism as Hallmarks for Innate Immune Cell Activation and Function.

Zhao, Haoxin / Raines, Lydia N / Huang, Stanley Ching-Cheng

Cells

2020 Volume 9, Issue 3

Abstract: Immune activation is now understood to be fundamentally linked to intrinsic and/or extrinsic metabolic processes which are essential for immune cells to survive, proliferate, and perform their effector functions. Moreover, disruption or dysregulation of ... ...

Abstract	Immune activation is now understood to be fundamentally linked to intrinsic and/or extrinsic metabolic processes which are essential for immune cells to survive, proliferate, and perform their effector functions. Moreover, disruption or dysregulation of these pathways can result in detrimental outcomes and underly a number of pathologies in both communicable and non-communicable diseases. In this review, we discuss how the metabolism of carbohydrates and amino acids in particular can modulate innate immunity and how perturbations in these pathways can result in failure of these immune cells to properly function or induce unfavorable phenotypes.
MeSH term(s)	Amino Acids/metabolism ; Animals ; Carbohydrate Metabolism ; Humans ; Immunity, Innate ; Models, Biological ; Myeloid-Derived Suppressor Cells/metabolism
Chemical Substances	Amino Acids
Language	English
Publishing date	2020-02-27
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells9030562
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Article ; Online: Circles of Life: linking metabolic and epigenetic cycles to immunity.

Lio, Chan-Wang Jerry / Huang, Stanley Ching-Cheng

Immunology

2020 Volume 161, Issue 3, Page(s) 165–174

Abstract: Metabolites are the essential substrates for epigenetic modification enzymes to write or erase the epigenetic blueprint in cells. Hence, the availability of nutrients and activity of metabolic pathways strongly influence the enzymatic function. Recent ... ...

Abstract	Metabolites are the essential substrates for epigenetic modification enzymes to write or erase the epigenetic blueprint in cells. Hence, the availability of nutrients and activity of metabolic pathways strongly influence the enzymatic function. Recent studies have shed light on the choreography between metabolome and epigenome in the control of immune cell differentiation and function, with a major focus on histone modifications. Yet, despite its importance in gene regulation, DNA methylation and its relationship with metabolism is relatively unclear. In this review, we will describe how the metabolic flux can influence epigenetic networks in innate and adaptive immune cells, with a focus on the DNA methylation cycle and the metabolites S-adenosylmethionine and α-ketoglutarate. Future directions will be discussed for this rapidly emerging field.
MeSH term(s)	Adaptive Immunity ; Animals ; Citric Acid Cycle/immunology ; DNA Methylation ; Epigenesis, Genetic ; Epigenome/immunology ; Humans ; Immunity, Innate ; Ketoglutaric Acids/metabolism ; Metabolome/immunology ; S-Adenosylmethionine/metabolism
Chemical Substances	Ketoglutaric Acids ; S-Adenosylmethionine (7LP2MPO46S)
Keywords	covid19
Language	English
Publishing date	2020-06-03
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80124-0
ISSN	1365-2567 ; 0019-2805 ; 0953-4954
ISSN (online)	1365-2567
ISSN	0019-2805 ; 0953-4954
DOI	10.1111/imm.13207
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Ud II Zs.181: Show issues

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Article ; Online: Fatty acids secreted from head and neck cancer induce M2-like Macrophages.

Albakri, Marwah M / Huang, Stanley Ching-Cheng / Tashkandi, Hammad N / Sieg, Scott F

Journal of leukocyte biology

2022 Volume 112, Issue 4, Page(s) 617–628

Abstract: Tumor-infiltrating monocytes can mature into Macrophages that support tumor survival or that display antitumor properties. To explore mechanisms steering Macrophage maturation, we assessed the effects of supernatants from squamous cell carcinoma cell ... ...

Abstract	Tumor-infiltrating monocytes can mature into Macrophages that support tumor survival or that display antitumor properties. To explore mechanisms steering Macrophage maturation, we assessed the effects of supernatants from squamous cell carcinoma cell lines (FaDu and SCC) on monocyte-derived Macrophage maturation. Purified monocytes were incubated in medium or medium supplemented with supernatants from FaDu and SCC9 or the leukemia monocytic cell line, THP-1. Macrophages were examined for markers of maturation (CD14, CD68), activation (HLA-DR, CD86, IL15R), scavenger receptor (CD36), toll-like receptor (TLR4), M2 marker (CD206), immune checkpoint (PD-L1), and intracellular chemokine expression (IP-10). Compared to other conditions, cells incubated with FaDu or SCC9 supernatants displayed enhanced survival, down-regulation of cell surface HLA-DR, CD86, IL-15R, CD36, and intracellular IP-10 expression, and increased cell surface PD-L1, CD14, and CD206 expression. Despite expressing TLR4 and CD14, Macrophages matured in tumor supernatants failed to respond to stimulation with the canonical TLR4 agonist, LPS. These changes were accompanied by a decrease in intracellular phospho-p38 expression in tumor supernatant conditioned Macrophages. Depletion of fatty acids from tumor supernatants or treatment of cell cultures with an inhibitor of fatty acid oxidation, Etomoxir, reversed a number of these phenotypic changes induced by tumor supernatants. Additionally, Macrophages incubated with either palmitic acid or oleic acid developed similar phenotypes as cells incubated in tumor supernatants. Together, these data suggest that fatty acids derived from tumor cells can mediate the maturation of Macrophages into a cell type with limited pro-inflammatory characteristics.
MeSH term(s)	B7-H1 Antigen/metabolism ; Chemokine CXCL10/metabolism ; Fatty Acids/metabolism ; HLA-DR Antigens/metabolism ; Head and Neck Neoplasms ; Humans ; Lipopolysaccharides/pharmacology ; Macrophages/metabolism ; Oleic Acids/metabolism ; Oleic Acids/pharmacology ; Palmitic Acids/metabolism ; Palmitic Acids/pharmacology ; Toll-Like Receptor 4/metabolism
Chemical Substances	B7-H1 Antigen ; Chemokine CXCL10 ; Fatty Acids ; HLA-DR Antigens ; Lipopolysaccharides ; Oleic Acids ; Palmitic Acids ; Toll-Like Receptor 4
Language	English
Publishing date	2022-02-25
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	605722-6
ISSN	1938-3673 ; 0741-5400
ISSN (online)	1938-3673
ISSN	0741-5400
DOI	10.1002/JLB.1A0521-251R
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Article ; Online: Navigating metabolic pathways to enhance antitumour immunity and immunotherapy.

Li, Xiaoyun / Wenes, Mathias / Romero, Pedro / Huang, Stanley Ching-Cheng / Fendt, Sarah-Maria / Ho, Ping-Chih

Nature reviews. Clinical oncology

2019 Volume 16, Issue 7, Page(s) 425–441

Abstract: The development of immunotherapies over the past decade has resulted in a paradigm shift in the treatment of cancer. However, the majority of patients do not benefit from immunotherapy, presumably owing to insufficient reprogramming of the ... ...

Abstract	The development of immunotherapies over the past decade has resulted in a paradigm shift in the treatment of cancer. However, the majority of patients do not benefit from immunotherapy, presumably owing to insufficient reprogramming of the immunosuppressive tumour microenvironment (TME) and thus limited reinvigoration of antitumour immunity. Various metabolic machineries and nutrient-sensing mechanisms orchestrate the behaviour of immune cells in response to nutrient availability in the TME. Notably, tumour-infiltrating immune cells typically experience metabolic stress as a result of the dysregulated metabolic activity of tumour cells, leading to impaired antitumour immune responses. Moreover, the immune checkpoints that are often exploited by tumour cells to evade immunosurveillance have emerging roles in modulating the metabolic and functional activity of T cells. Thus, repurposing of drugs targeting cancer metabolism might synergistically enhance immunotherapy via metabolic reprogramming of the TME. In addition, interventions targeting the metabolic circuits that impede antitumour immunity have been developed, with several clinical trials underway. Herein, we discuss how these metabolic circuits regulate antitumour immunity and the possible approaches to targeting these pathways in the context of anticancer immunotherapy. We also describe hypothetical combination treatments that could be used to better unleash the potential of adoptive cell therapies by enhancing T cell metabolism.
MeSH term(s)	Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Combined Modality Therapy ; Drug Repositioning ; Drug Synergism ; Humans ; Immunotherapy/methods ; Metabolic Networks and Pathways/drug effects ; Neoplasms/drug therapy ; Neoplasms/immunology ; Tumor Microenvironment/drug effects
Chemical Substances	Antineoplastic Agents
Language	English
Publishing date	2019-03-26
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2491410-1
ISSN	1759-4782 ; 1759-4774
ISSN (online)	1759-4782
ISSN	1759-4774
DOI	10.1038/s41571-019-0203-7
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Zs.A 6029: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MG 103: Show issues

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Article ; Online: ILC3s integrate glycolysis and mitochondrial production of reactive oxygen species to fulfill activation demands.

Di Luccia, Blanda / Gilfillan, Susan / Cella, Marina / Colonna, Marco / Huang, Stanley Ching-Cheng

The Journal of experimental medicine

2019 Volume 216, Issue 10, Page(s) 2231–2241

Abstract: Group 3 innate lymphoid cells (ILC3s) are the innate counterparts of Th17 that require the transcription factor RORγt for development and contribute to the defense against pathogens through IL-22 and IL-17 secretion. Proliferation and effector functions ... ...

Abstract	Group 3 innate lymphoid cells (ILC3s) are the innate counterparts of Th17 that require the transcription factor RORγt for development and contribute to the defense against pathogens through IL-22 and IL-17 secretion. Proliferation and effector functions of Th17 require a specific mTOR-dependent metabolic program that utilizes high-rate glycolysis, while mitochondrial lipid oxidation and production of reactive oxygen species (mROS) support alternative T reg cell differentiation. Whether ILC3s employ a specific metabolic program is not known. Here, we find that ILC3s rely on mTOR complex 1 (mTORC1) for proliferation and production of IL-22 and IL-17A after in vitro activation and
MeSH term(s)	Animals ; Citrobacter rodentium/immunology ; Enterobacteriaceae Infections/genetics ; Enterobacteriaceae Infections/immunology ; Enterobacteriaceae Infections/pathology ; Glycolysis/genetics ; Glycolysis/immunology ; Hypoxia-Inducible Factor 1, alpha Subunit/genetics ; Hypoxia-Inducible Factor 1, alpha Subunit/immunology ; Interleukin-17/genetics ; Interleukin-17/immunology ; Interleukins/genetics ; Interleukins/immunology ; Lymphocyte Activation ; Mechanistic Target of Rapamycin Complex 1/genetics ; Mechanistic Target of Rapamycin Complex 1/immunology ; Mice ; Mice, Knockout ; Mitochondria/genetics ; Mitochondria/immunology ; Mitochondria/pathology ; Nuclear Receptor Subfamily 1, Group F, Member 3/genetics ; Nuclear Receptor Subfamily 1, Group F, Member 3/immunology ; Reactive Oxygen Species/immunology ; Th17 Cells/immunology ; Th17 Cells/pathology ; Interleukin-22
Chemical Substances	Hif1a protein, mouse ; Hypoxia-Inducible Factor 1, alpha Subunit ; Il17a protein, mouse ; Interleukin-17 ; Interleukins ; Nuclear Receptor Subfamily 1, Group F, Member 3 ; Reactive Oxygen Species ; Rorc protein, mouse ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1)
Language	English
Publishing date	2019-07-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20180549
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Zs.MG 45: Show issues

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