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Article ; Online: Engineered bacteria recycle tumor metabolic waste to boost immunotherapy.

Cubillos-Ruiz, Juan R / Cubillos-Ruiz, Andres

2021 Volume 29, Issue 12, Page(s) 1725–1727

Abstract: A recent study published in Nature by Canale et al. (2021) shows that engineered probiotic bacteria can be used to augment the availability of nutrients required for optimal immune cell function in tumors. This approach enhances anti-tumor immunity and ... ...

Abstract	A recent study published in Nature by Canale et al. (2021) shows that engineered probiotic bacteria can be used to augment the availability of nutrients required for optimal immune cell function in tumors. This approach enhances anti-tumor immunity and improves the efficacy of immunotherapy in mouse models of cancer.
MeSH term(s)	Animals ; Bacteria/genetics ; Bacteria/metabolism ; Disease Models, Animal ; Immunization, Secondary ; Immunotherapy ; Metabolic Engineering ; Mice ; Neoplasms/metabolism ; Nutrients ; Probiotics ; Tumor Microenvironment/immunology
Language	English
Publishing date	2021-12-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	2278004-X
ISSN	1934-6069 ; 1931-3128
ISSN (online)	1934-6069
ISSN	1931-3128
DOI	10.1016/j.chom.2021.11.008
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Zs.A 6578: Show issues

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Article ; Online: Optineurin Guards IFNγ Signaling in Cancer Cells.

Salvagno, Camilla / Cubillos-Ruiz, Juan R

Cancer discovery

2021 Volume 11, Issue 7, Page(s) 1623–1625

Abstract: In this issue, Du and colleagues uncover that optineurin functions as a key regulator of IFNγ receptor (IFNGR1) stability in malignant cells. Loss of optineurin in colorectal cancer cells causes IFNGR1 degradation, leading to impaired IFNγ signaling, ... ...

Abstract	In this issue, Du and colleagues uncover that optineurin functions as a key regulator of IFNγ receptor (IFNGR1) stability in malignant cells. Loss of optineurin in colorectal cancer cells causes IFNGR1 degradation, leading to impaired IFNγ signaling, decreased MHC-I expression, and enhanced ability to evade adaptive immune control.
MeSH term(s)	Neoplasms/genetics ; Receptors, Interferon
Chemical Substances	Receptors, Interferon
Language	English
Publishing date	2021-07-18
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	2625242-9
ISSN	2159-8290 ; 2159-8274
ISSN (online)	2159-8290
ISSN	2159-8274
DOI	10.1158/2159-8290.CD-21-0362
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Zs.A 6916: Show issues

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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: Endoplasmic reticulum stress signals in the tumour and its microenvironment.

Chen, Xi / Cubillos-Ruiz, Juan R

Nature reviews. Cancer

2020 Volume 21, Issue 2, Page(s) 71–88

Abstract: Protein handling, modification and folding in the endoplasmic reticulum (ER) are tightly regulated processes that determine cell function, fate and survival. In several tumour types, diverse oncogenic, transcriptional and metabolic abnormalities ... ...

Abstract	Protein handling, modification and folding in the endoplasmic reticulum (ER) are tightly regulated processes that determine cell function, fate and survival. In several tumour types, diverse oncogenic, transcriptional and metabolic abnormalities cooperate to generate hostile microenvironments that disrupt ER homeostasis in malignant and stromal cells, as well as infiltrating leukocytes. These changes provoke a state of persistent ER stress that has been demonstrated to govern multiple pro-tumoural attributes in the cancer cell while dynamically reprogramming the function of innate and adaptive immune cells. Aberrant activation of ER stress sensors and their downstream signalling pathways have therefore emerged as key regulators of tumour growth and metastasis as well as response to chemotherapy, targeted therapies and immunotherapy. In this Review, we discuss the physiological inducers of ER stress in the tumour milieu, the interplay between oncogenic signalling and ER stress response pathways in the cancer cell and the profound immunomodulatory effects of sustained ER stress responses in tumours.
MeSH term(s)	Animals ; Disease Models, Animal ; Endoplasmic Reticulum/immunology ; Endoplasmic Reticulum/physiology ; Endoplasmic Reticulum Stress/immunology ; Endoplasmic Reticulum Stress/physiology ; Humans ; Immunomodulation/immunology ; Immunomodulation/physiology ; Neoplasms/immunology ; Neoplasms/physiopathology ; Neoplastic Processes ; Signal Transduction/immunology ; Signal Transduction/physiology ; Tumor Microenvironment/immunology ; Tumor Microenvironment/physiology ; Unfolded Protein Response/immunology ; Unfolded Protein Response/physiology
Language	English
Publishing date	2020-11-19
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	2062767-1
ISSN	1474-1768 ; 1474-175X
ISSN (online)	1474-1768
ISSN	1474-175X
DOI	10.1038/s41568-020-00312-2
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Zs.A 5563: 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 24: Show issues

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Article ; Online: Decoding endoplasmic reticulum stress signals in cancer cells and antitumor immunity.

Salvagno, Camilla / Mandula, Jessica K / Rodriguez, Paulo C / Cubillos-Ruiz, Juan R

Trends in cancer

2022 Volume 8, Issue 11, Page(s) 930–943

Abstract: ... activating transcription factor (ATF6), inositol-requiring enzyme 1α (IRE1α), and protein kinase R (PKR)-like ER kinase (PERK ...

Abstract	The tumor microenvironment (TME) provokes endoplasmic reticulum (ER) stress in malignant cells and infiltrating immune populations. Sensing and responding to ER stress is coordinated by the unfolded protein response (UPR), an integrated signaling pathway governed by three ER stress sensors: activating transcription factor (ATF6), inositol-requiring enzyme 1α (IRE1α), and protein kinase R (PKR)-like ER kinase (PERK). Persistent UPR activation modulates malignant progression, tumor growth, metastasis, and protective antitumor immunity. Hence, therapies targeting ER stress signaling can be harnessed to elicit direct tumor killing and concomitant anticancer immunity. We highlight recent findings on the role of the ER stress responses in onco-immunology, with an emphasis on genetic vulnerabilities that render tumors highly sensitive to therapeutic UPR modulation.
MeSH term(s)	Humans ; Endoplasmic Reticulum Stress ; Endoribonucleases/metabolism ; Protein Serine-Threonine Kinases ; Neoplasms/pathology ; Inositol ; Tumor Microenvironment
Chemical Substances	Endoribonucleases (EC 3.1.-) ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Inositol (4L6452S749)
Language	English
Publishing date	2022-07-08
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2852626-0
ISSN	2405-8025 ; 2405-8033 ; 2405-8033
ISSN (online)	2405-8025 ; 2405-8033
ISSN	2405-8033
DOI	10.1016/j.trecan.2022.06.006
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Article ; Online: Endoplasmic Reticulum Stress Responses in Intratumoral Immune Cells: Implications for Cancer Immunotherapy.

Song, Minkyung / Cubillos-Ruiz, Juan R

Trends in immunology

2019 Volume 40, Issue 2, Page(s) 128–141

Abstract: Protective anti-tumor immune responses are mediated by effector molecules that enable successful elimination of malignant cells. As the site where transmembrane and secreted proteins are generated, the endoplasmic reticulum (ER) of immune cells plays a ... ...

Abstract	Protective anti-tumor immune responses are mediated by effector molecules that enable successful elimination of malignant cells. As the site where transmembrane and secreted proteins are generated, the endoplasmic reticulum (ER) of immune cells plays a key role in this process. Recent studies have indicated that adverse conditions within tumors perturb ER homeostasis in infiltrating immune cells, which can impede the development of effective anti-cancer immunity. Here, we describe how the tumor microenvironment induces ER stress in immune cells, and discuss the detrimental consequences of persistent ER stress responses in intratumoral immune populations. We also explore the concept of targeting ER stress responses to reinvigorate endogenous anti-tumor immunity and enhance the efficacy of various forms of cancer immunotherapy.
MeSH term(s)	Animals ; Endoplasmic Reticulum Stress/immunology ; Humans ; Immunotherapy ; Neoplasms/immunology ; Neoplasms/pathology ; Neoplasms/therapy
Language	English
Publishing date	2019-01-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	2036831-8
ISSN	1471-4981 ; 1471-4906
ISSN (online)	1471-4981
ISSN	1471-4906
DOI	10.1016/j.it.2018.12.001
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Zs.A 1601: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 2: Show issues

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Article: The impact of endoplasmic reticulum stress responses in dendritic cell immunobiology.

Salvagno, Camilla / Cubillos-Ruiz, Juan R

International review of cell and molecular biology

2019 Volume 349, Page(s) 153–176

Abstract: Dendritic cells (DCs) are critical for bridging innate and adaptive immunity. They do so by presenting antigens to T cells, and by expressing diverse molecules that further promote T cell activation, differentiation and memory formation. During this ... ...

Abstract	Dendritic cells (DCs) are critical for bridging innate and adaptive immunity. They do so by presenting antigens to T cells, and by expressing diverse molecules that further promote T cell activation, differentiation and memory formation. During this process, intracellular and extracellular factors can perturb the protein-folding capacity of endoplasmic reticulum (ER) and induce a cellular state of "ER stress," which is controlled and resolved by the unfolded protein response (UPR). Interestingly, various studies have shown that DCs can activate UPR-related pathways even in the absence of global ER stress, and that this process can modulate their normal activity. In other settings, such as cancer, adverse microenvironmental conditions have been demonstrated to evoke severe ER stress and persistent activation of the UPR in tumor-infiltrating DCs. This process disrupts their metabolism and local antigen-presenting capacity, hence impeding the initiation and maintenance of anti-cancer immunity. Here, we review recent findings on how canonical and non-canonical UPR activation impacts DC immunobiology at the steady-state, upon activation via pattern recognition receptors, and under diverse pathological conditions. We also discuss the potential therapeutic implications that targeting the UPR in DCs may have in the context of cancer and in other pathologies such as graft-versus-host disease.
MeSH term(s)	Animals ; Dendritic Cells/immunology ; Dendritic Cells/pathology ; Endoplasmic Reticulum Stress/immunology ; Humans ; Unfolded Protein Response
Language	English
Publishing date	2019-09-11
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	2427220-6
ISSN	1937-6448 ; 0074-7696
ISSN	1937-6448 ; 0074-7696
DOI	10.1016/bs.ircmb.2019.08.004
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Uc I Zs.317: Show issues

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Article ; Online: Dendritic Cell Metabolism and Function in Tumors.

Giovanelli, Paolo / Sandoval, Tito A / Cubillos-Ruiz, Juan R

Trends in immunology

2019 Volume 40, Issue 8, Page(s) 699–718

Abstract: Dendritic cells (DCs) are fundamental for the initiation and maintenance of immune responses against malignant cells. Despite the unique potential of DCs to elicit robust anticancer immunity, the tumor microenvironment poses a variety of challenges that ... ...

Abstract	Dendritic cells (DCs) are fundamental for the initiation and maintenance of immune responses against malignant cells. Despite the unique potential of DCs to elicit robust anticancer immunity, the tumor microenvironment poses a variety of challenges that hinder competent DC function and consequently inhibit the development of protective immune responses. Here, we discuss recent studies uncovering new molecular pathways and metabolic programs that tumors manipulate in DCs to disturb their homeostasis and evade immune control. We also examine certain state-of-the-art strategies that seek to improve DC function and elicit antitumor responses in hosts with cancer. Understanding and modulating DC metabolism and activity within tumors might help improve the efficacy of T cell-centric immunotherapies.
MeSH term(s)	Amino Acids/metabolism ; Animals ; Cellular Reprogramming ; Dendritic Cells/immunology ; Dendritic Cells/metabolism ; Disease Susceptibility/immunology ; Energy Metabolism ; Glycolysis ; Humans ; Immunomodulation ; Lipid Metabolism ; Mice ; Neoplasms/etiology ; Neoplasms/metabolism ; Neoplasms/pathology ; Nitric Oxide/metabolism ; Nitric Oxide Synthase Type II/metabolism ; Oxidative Stress ; T-Lymphocyte Subsets/immunology ; T-Lymphocyte Subsets/metabolism ; Tumor Microenvironment/immunology
Chemical Substances	Amino Acids ; Nitric Oxide (31C4KY9ESH) ; Nitric Oxide Synthase Type II (EC 1.14.13.39)
Language	English
Publishing date	2019-07-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	2036831-8
ISSN	1471-4981 ; 1471-4906
ISSN (online)	1471-4981
ISSN	1471-4906
DOI	10.1016/j.it.2019.06.004
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Zs.A 1601: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 2: Show issues

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Article ; Online: Remodeling of the Enterococcal Cell Envelope during Surface Penetration Promotes Intrinsic Resistance to Stress.

Ramos, Yusibeska / Sansone, Stephanie / Hwang, Sung-Min / Sandoval, Tito A / Zhu, Mengmeng / Zhang, Guoan / Cubillos-Ruiz, Juan R / Morales, Diana K

mBio

2022 Volume 13, Issue 6, Page(s) e0229422

Abstract: Enterococcus faecalis is a normal commensal of the human gastrointestinal tract (GIT). However, upon disruption of gut homeostasis, this nonmotile bacterium can egress from its natural niche and spread to distal organs. While this translocation process ... ...

Abstract	Enterococcus faecalis is a normal commensal of the human gastrointestinal tract (GIT). However, upon disruption of gut homeostasis, this nonmotile bacterium can egress from its natural niche and spread to distal organs. While this translocation process can lead to life-threatening systemic infections, the underlying mechanisms remain largely unexplored. Our prior work showed that E. faecalis migration across diverse surfaces requires the formation of matrix-covered multicellular aggregates and the synthesis of exopolysaccharides, but how enterococcal cells are reprogrammed during this process is unknown. Whether surface penetration endows E. faecalis with adaptive advantages is also uncertain. Here, we report that surface penetration promotes the generation of a metabolically and phenotypically distinct E. faecalis population with an enhanced capacity to endure various forms of extracellular stress. Surface-invading enterococci demonstrated major ultrastructural alterations in their cell envelope characterized by increased membrane glycolipid content. These changes were accompanied by marked induction of specific transcriptional programs enhancing cell envelope biogenesis and glycolipid metabolism. Notably, the surface-invading population demonstrated superior tolerance to membrane-damaging antimicrobials, including daptomycin and β-defensins produced by epithelial cells. Genetic mutations impairing glycolipid biosynthesis sensitized E. faecalis to envelope stressors and reduced the ability of this bacterium to penetrate semisolid surfaces and translocate through human intestinal epithelial cell monolayers. Our study reveals that surface penetration induces distinct transcriptional, metabolic, and ultrastructural changes that equip E. faecalis with enhanced capacity to resist external stressors and thrive in its surrounding environment.
MeSH term(s)	Humans ; Cell Membrane/metabolism ; Daptomycin/pharmacology ; Cell Wall/metabolism ; Enterococcus faecalis/genetics ; Biofilms ; Anti-Bacterial Agents/pharmacology
Chemical Substances	Daptomycin (NWQ5N31VKK) ; Anti-Bacterial Agents
Language	English
Publishing date	2022-11-10
Publishing country	United States
Document type	Journal Article
ZDB-ID	2557172-2
ISSN	2150-7511 ; 2161-2129
ISSN (online)	2150-7511
ISSN	2161-2129
DOI	10.1128/mbio.02294-22
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Article: Methods and protocols for chemotherapy-induced peripheral neuropathy (CIPN) mouse models using paclitaxel.

Pennypacker, Sarah D / Fonseca, Miriam M / Morgan, James W / Dougherty, Patrick M / Cubillos-Ruiz, Juan R / Strowd, Roy E / Romero-Sandoval, E Alfonso

Methods in cell biology

2022 Volume 168, Page(s) 277–298

Abstract: While cancer patients may have chemotherapeutics to thank for being cured of their malignancy, they are often left to suffer a disabling neuropathy induced by that same cancer treatment. This neuropathy, known as chemotherapy-induced peripheral ... ...

Abstract	While cancer patients may have chemotherapeutics to thank for being cured of their malignancy, they are often left to suffer a disabling neuropathy induced by that same cancer treatment. This neuropathy, known as chemotherapy-induced peripheral neuropathy, or CIPN, is one of the most debilitating survivorship concerns for patients, with many citing hallmark symptoms of hyperalgesia, allodynia, and numbness, and subsequently reducing their dose or even ceasing treatment altogether. Investigations into this interplay between the antineoplastic activity of chemotherapeutic agents and the preservation of peripheral nerve health are therefore crucial for the development of CIPN treatment and prevention methods. Responding to need, current literature is inundated with varying preclinical models of CIPN. This chapter thus seeks to provide a detailed and reliable methodology for the induction and assessment of CIPN in mice, using a preclinical model that is both reproducible and translatable to several aspects of the clinical phenotype. Specifically, this chapter lays out a model for intermittent low-dose paclitaxel induction of CIPN in C57BL/6J mice, and a testing of this induction via von Frey filament mechanical hypersensitivity assays, a mechanical hyposensitivity (numbness) assay, and a cold-thermal allodynia assay (acetone test). These protocols can easily be adjusted to fit the needs of individual CIPN experiments, as stated throughout the chapter.
MeSH term(s)	Animals ; Antineoplastic Agents/toxicity ; Humans ; Hyperalgesia/chemically induced ; Hyperalgesia/drug therapy ; Hyperalgesia/genetics ; Mice ; Mice, Inbred C57BL ; Paclitaxel/adverse effects ; Peripheral Nervous System Diseases/chemically induced ; Peripheral Nervous System Diseases/drug therapy
Chemical Substances	Antineoplastic Agents ; Paclitaxel (P88XT4IS4D)
Language	English
Publishing date	2022-01-10
Publishing country	United States
Document type	Journal Article
ISSN	0091-679X
ISSN	0091-679X
DOI	10.1016/bs.mcb.2021.12.019
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