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Article ; Online: Editorial: Knocking on neuroimmunology's doors: an entrechat concerning the immune system balance and its cell metabolism orchestration.

Sambucci, Manolo / Dardalhon, Valérie / Latorre, Daniela

2023 Volume 14, Page(s) 1236217

Language	English
Publishing date	2023-06-26
Publishing country	Switzerland
Document type	Editorial
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2023.1236217
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Article ; Online: Targeting Glutamine Metabolism and PD-L1: A Novel Anti-tumor Pas de Deux.

Matias, Maria I / Dardalhon, Valérie / Taylor, Naomi

Molecular cell

2020 Volume 80, Issue 4, Page(s) 555–557

Abstract: In this issue of Molecular Cell, Byun et al. (2020) find that the dual targeting of glutamine metabolism and the PD-L1 checkpoint inhibitor augments anti-tumor immunity. Mechanistically, decreased glutamine availability attenuated S-glutathionylation of ... ...

Abstract	In this issue of Molecular Cell, Byun et al. (2020) find that the dual targeting of glutamine metabolism and the PD-L1 checkpoint inhibitor augments anti-tumor immunity. Mechanistically, decreased glutamine availability attenuated S-glutathionylation of SERCA, resulting in an increase in cytosolic calcium, enhanced NF-κB activity, and upregulation of programmed death-ligand 1.
MeSH term(s)	B7-H1 Antigen/genetics ; Glutamine ; Humans ; NF-kappa B/genetics ; Neoplasms/drug therapy ; Neoplasms/genetics
Chemical Substances	B7-H1 Antigen ; NF-kappa B ; Glutamine (0RH81L854J)
Language	English
Publishing date	2020-11-20
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	1415236-8
ISSN	1097-4164 ; 1097-2765
ISSN (online)	1097-4164
ISSN	1097-2765
DOI	10.1016/j.molcel.2020.11.005
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Article ; Online: Single-Molecule DNA Methylation Reveals Unique Epigenetic Identity Profiles of T Helper Cells.

Goldsmith, Chloe / Thevin, Valentin / Fesneau, Olivier / Matias, Maria I / Perrault, Julie / Abid, Ali Hani / Taylor, Naomi / Dardalhon, Valérie / Marie, Julien C / Hernandez-Vargas, Hector

Journal of immunology (Baltimore, Md. : 1950)

2024 Volume 212, Issue 6, Page(s) 1029–1039

Abstract: Both identity and plasticity of CD4 T helper (Th) cells are regulated in part by epigenetic mechanisms. However, a method that reliably and readily profiles DNA base modifications is still needed to finely study Th cell differentiation. Cytosine ... ...

Abstract	Both identity and plasticity of CD4 T helper (Th) cells are regulated in part by epigenetic mechanisms. However, a method that reliably and readily profiles DNA base modifications is still needed to finely study Th cell differentiation. Cytosine methylation in CpG context (5mCpG) and cytosine hydroxymethylation (5hmCpG) are DNA modifications that identify stable cell phenotypes, but their potential to characterize intermediate cell transitions has not yet been evaluated. To assess transition states in Th cells, we developed a method to profile Th cell identity using Cas9-targeted single-molecule nanopore sequencing. Targeting as few as 10 selected genomic loci, we were able to distinguish major in vitro polarized murine T cell subtypes, as well as intermediate phenotypes, by their native DNA 5mCpG patterns. Moreover, by using off-target sequences, we were able to infer transcription factor activities relevant to each cell subtype. Detection of 5mCpG and 5hmCpG was validated on intestinal Th17 cells escaping transforming growth factor β control, using single-molecule adaptive sampling. A total of 21 differentially methylated regions mapping to the 10-gene panel were identified in pathogenic Th17 cells relative to their nonpathogenic counterpart. Hence, our data highlight the potential to exploit native DNA methylation profiling to study physiological and pathological transition states of Th cells.
MeSH term(s)	Animals ; Mice ; DNA Methylation ; Epigenesis, Genetic ; Cytosine ; DNA/metabolism ; Th17 Cells/metabolism
Chemical Substances	Cytosine (8J337D1HZY) ; DNA (9007-49-2)
Language	English
Publishing date	2024-01-29
Publishing country	United States
Document type	Journal Article
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.2300091
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Article: Targeting Glutamine Metabolism and PD-L1: A Novel Anti-tumor Pas de Deux

Matias, Maria I / Dardalhon, Valérie / Taylor, Naomi

Molecular cell. 2020 Nov. 19, v. 80, no. 4

2020

Abstract	In this issue of Molecular Cell, Byun et al. (2020) find that the dual targeting of glutamine metabolism and the PD-L1 checkpoint inhibitor augments anti-tumor immunity. Mechanistically, decreased glutamine availability attenuated S-glutathionylation of SERCA, resulting in an increase in cytosolic calcium, enhanced NF-κB activity, and upregulation of programmed death-ligand 1.
Keywords	calcium ; glutamine ; immunity ; metabolism
Language	English
Dates of publication	2020-1119
Size	p. 555-557.
Publishing place	Elsevier Inc.
Document type	Article
Note	NAL-AP-2-clean
ZDB-ID	1415236-8
ISSN	1097-4164 ; 1097-2765
ISSN (online)	1097-4164
ISSN	1097-2765
DOI	10.1016/j.molcel.2020.11.005
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Glutamine promotes the generation of B10

Mielle, Julie / Morel, Jacques / Elhmioui, Jamila / Combe, Bernard / Macia, Laurence / Dardalhon, Valérie / Taylor, Naomi / Audo, Rachel / Daien, Claire

European journal of immunology

2022 Volume 52, Issue 3, Page(s) 418–430

Abstract: Alterations in cell metabolism can shift the differentiation of immune cells toward a regulatory or inflammatory phenotype, thus, opening up new therapeutic opportunities for immune-related diseases. Indeed, growing knowledge on T- cell metabolism has ... ...

Abstract	Alterations in cell metabolism can shift the differentiation of immune cells toward a regulatory or inflammatory phenotype, thus, opening up new therapeutic opportunities for immune-related diseases. Indeed, growing knowledge on T- cell metabolism has revealed differences in the metabolic programs of suppressive Tregs as compared to inflammatory Th1 and Th17 cells. In addition to Tregs, IL-10-producing regulatory B cells are crucial for maintaining tolerance, inhibiting inflammation, and autoimmunity. Yet, the metabolic networks regulating diverse B-lymphocyte responses are not well known. Here, we show that glutaminase blockade decreased downstream mTOR activation and attenuated IL-10 secretion. Direct suppression of mTOR activity by rapamycin selectively impaired IL-10 production by B cells whereas secretion was restored upon Glycogen synthase kinase 3 (GSK3) inhibition. Mechanistically, we found mTORC1 activation leads to GSK3 inhibition, identifying a key signalling pathway regulating IL-10 secretion by B lymphocytes. Thus, our results identify glutaminolysis and the mTOR/GSK3 signalling axis, as critical regulators of the generation of IL-10 producing B cells with regulatory functions.
MeSH term(s)	B-Lymphocytes, Regulatory ; Glutamine/metabolism ; Glycogen Synthase Kinase 3 ; Interleukin-10/metabolism ; TOR Serine-Threonine Kinases/metabolism
Chemical Substances	Glutamine (0RH81L854J) ; Interleukin-10 (130068-27-8) ; TOR Serine-Threonine Kinases (EC 2.7.11.1) ; Glycogen Synthase Kinase 3 (EC 2.7.11.26)
Language	English
Publishing date	2022-02-01
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	120108-6
ISSN	1521-4141 ; 0014-2980
ISSN (online)	1521-4141
ISSN	0014-2980
DOI	10.1002/eji.202149387
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Article ; Online: Tuft cell acetylcholine is released into the gut lumen to promote anti-helminth immunity.

Ndjim, Marième / Gasmi, Imène / Herbert, Fabien / Joséphine, Charlène / Bas, Julie / Lamrani, Ali / Coutry, Nathalie / Henry, Sylvain / Zimmermann, Valérie S / Dardalhon, Valérie / Campillo Poveda, Marta / Turtoi, Evgenia / Thirard, Steeve / Forichon, Luc / Giordano, Alicia / Ciancia, Claire / Homayed, Zeinab / Pannequin, Julie / Britton, Collette /

Devaney, Eileen / McNeilly, Tom N / Berrard, Sylvie / Turtoi, Andrei / Maizels, Rick M / Gerbe, François / Jay, Philippe

Immunity

2024

Abstract: Upon parasitic helminth infection, activated intestinal tuft cells secrete interleukin-25 (IL-25), which initiates a type 2 immune response during which lamina propria type 2 innate lymphoid cells (ILC2s) produce IL-13. This causes epithelial remodeling, ...

Abstract	Upon parasitic helminth infection, activated intestinal tuft cells secrete interleukin-25 (IL-25), which initiates a type 2 immune response during which lamina propria type 2 innate lymphoid cells (ILC2s) produce IL-13. This causes epithelial remodeling, including tuft cell hyperplasia, the function of which is unknown. We identified a cholinergic effector function of tuft cells, which are the only epithelial cells that expressed choline acetyltransferase (ChAT). During parasite infection, mice with epithelial-specific deletion of ChAT had increased worm burden, fitness, and fecal egg counts, even though type 2 immune responses were comparable. Mechanistically, IL-13-amplified tuft cells release acetylcholine (ACh) into the gut lumen. Finally, we demonstrated a direct effect of ACh on worms, which reduced their fecundity via helminth-expressed muscarinic ACh receptors. Thus, tuft cells are sentinels in naive mice, and their amplification upon helminth infection provides an additional type 2 immune response effector function.
Language	English
Publishing date	2024-05-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	1217235-2
ISSN	1097-4180 ; 1074-7613
ISSN (online)	1097-4180
ISSN	1074-7613
DOI	10.1016/j.immuni.2024.04.018
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Article ; Online: Ras/MAPK signalling intensity defines subclonal fitness in a mouse model of hepatocellular carcinoma.

Lozano, Anthony / Souche, Francois-Régis / Chavey, Carine / Dardalhon, Valérie / Ramirez, Christel / Vegna, Serena / Desandre, Guillaume / Riviere, Anaïs / Zine El Aabidine, Amal / Fort, Philippe / Akkari, Leila / Hibner, Urszula / Grégoire, Damien

eLife

2023 Volume 12

Abstract: Quantitative differences in signal transduction are to date an understudied feature of tumour heterogeneity. The MAPK Erk pathway, which is activated in a large proportion of human tumours, is a prototypic example of distinct cell fates being driven by ... ...

Abstract	Quantitative differences in signal transduction are to date an understudied feature of tumour heterogeneity. The MAPK Erk pathway, which is activated in a large proportion of human tumours, is a prototypic example of distinct cell fates being driven by signal intensity. We have used primary hepatocyte precursors transformed with different dosages of an oncogenic form of Ras to model subclonal variations in MAPK signalling. Orthotopic allografts of Ras-transformed cells in immunocompromised mice gave rise to fast-growing aggressive tumours, both at the primary location and in the peritoneal cavity. Fluorescent labelling of cells expressing different oncogene levels, and consequently varying levels of MAPK Erk activation, highlighted the selection processes operating at the two sites of tumour growth. Indeed, significantly higher Ras expression was observed in primary as compared to secondary, metastatic sites, despite the apparent evolutionary trade-off of increased apoptotic death in the liver that correlated with high Ras dosage. Analysis of the immune tumour microenvironment at the two locations suggests that fast peritoneal tumour growth in the immunocompromised setting is abrogated in immunocompetent animals due to efficient antigen presentation by peritoneal dendritic cells. Furthermore, our data indicate that, in contrast to the metastatic-like outgrowth, strong MAPK signalling is required in the primary liver tumours to resist elimination by NK (natural killer) cells. Overall, this study describes a quantitative aspect of tumour heterogeneity and points to a potential vulnerability of a subtype of hepatocellular carcinoma as a function of MAPK Erk signalling intensity.
MeSH term(s)	Animals ; Humans ; Mice ; Carcinoma, Hepatocellular/genetics ; Killer Cells, Natural ; Liver Neoplasms/genetics ; MAP Kinase Signaling System ; Signal Transduction ; Tumor Microenvironment ; ras Proteins/metabolism
Chemical Substances	ras Proteins (EC 3.6.5.2)
Language	English
Publishing date	2023-01-19
Publishing country	England
Document type	Journal Article ; 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.76294
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Article ; Online: Ras/MAPK signalling intensity defines subclonal fitness in a mouse model of hepatocellular carcinoma

Anthony Lozano / Francois-Régis Souche / Carine Chavey / Valérie Dardalhon / Christel Ramirez / Serena Vegna / Guillaume Desandre / Anaïs Riviere / Amal Zine El Aabidine / Philippe Fort / Leila Akkari / Urszula Hibner / Damien Grégoire

eLife, Vol

2023 Volume 12

Abstract	Quantitative differences in signal transduction are to date an understudied feature of tumour heterogeneity. The MAPK Erk pathway, which is activated in a large proportion of human tumours, is a prototypic example of distinct cell fates being driven by signal intensity. We have used primary hepatocyte precursors transformed with different dosages of an oncogenic form of Ras to model subclonal variations in MAPK signalling. Orthotopic allografts of Ras-transformed cells in immunocompromised mice gave rise to fast-growing aggressive tumours, both at the primary location and in the peritoneal cavity. Fluorescent labelling of cells expressing different oncogene levels, and consequently varying levels of MAPK Erk activation, highlighted the selection processes operating at the two sites of tumour growth. Indeed, significantly higher Ras expression was observed in primary as compared to secondary, metastatic sites, despite the apparent evolutionary trade-off of increased apoptotic death in the liver that correlated with high Ras dosage. Analysis of the immune tumour microenvironment at the two locations suggests that fast peritoneal tumour growth in the immunocompromised setting is abrogated in immunocompetent animals due to efficient antigen presentation by peritoneal dendritic cells. Furthermore, our data indicate that, in contrast to the metastatic-like outgrowth, strong MAPK signalling is required in the primary liver tumours to resist elimination by NK (natural killer) cells. Overall, this study describes a quantitative aspect of tumour heterogeneity and points to a potential vulnerability of a subtype of hepatocellular carcinoma as a function of MAPK Erk signalling intensity.
Keywords	oncogenic dosage ; tumour heterogeneity ; microenvironment ; NK cells ; liver ; Medicine ; R ; Science ; Q ; Biology (General) ; QH301-705.5
Subject code	570
Language	English
Publishing date	2023-01-01T00:00:00Z
Publisher	eLife Sciences Publications Ltd
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Correction: Single amino-acid mutation in a Drosoph ila melanogaster ribosomal protein: An insight in uL11 transcriptional activity.

Grunchec, Héloïse / Deraze, Jérôme / Dardalhon-Cuménal, Delphine / Ribeiro, Valérie / Coléno-Costes, Anne / Dias, Karine / Bloyer, Sébastien / Mouchel-Vielh, Emmanuèle / Peronnet, Frédérique / Thomassin, Hélène

PloS one

2024 Volume 19, Issue 5, Page(s) e0304237

Abstract: This corrects the article DOI: 10.1371/journal.pone.0273198.]. ...

Abstract	[This corrects the article DOI: 10.1371/journal.pone.0273198.].
Language	English
Publishing date	2024-05-17
Publishing country	United States
Document type	Published Erratum
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0304237
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Article ; Online: Characterization of Th9 Cells in the Development of EAE and IBD.

Malik, Sakshi / Dardalhon, Valerie / Awasthi, Amit

Methods in molecular biology (Clifton, N.J.)

2017 Volume 1585, Page(s) 201–216

Abstract: Encephalitogenic and colitogenic effector T cells have been implicated in the induction of experimental autoimmune encephalomyelitis (EAE) and inflammatory bowel disease (IBD), respectively. Effector functions of Th1 and Th17 cells have been well ... ...

Abstract	Encephalitogenic and colitogenic effector T cells have been implicated in the induction of experimental autoimmune encephalomyelitis (EAE) and inflammatory bowel disease (IBD), respectively. Effector functions of Th1 and Th17 cells have been well characterized and described for the induction and development of EAE and IBD; however, the recently identified Th9 cells have also been suggested to play an important role in these autoimmune pathologies. Th9 cells, primarily characterized by their high level of production of IL-9, are not only essential in controlling extracellular pathogens but also contribute to the development of autoimmunity and allergic inflammation. Furthermore, it was also demonstrated that IL-9 promotes Th17 cell-mediated tissue pathology in EAE and it compromises the barrier functions of the gut in IBD. In vivo adoptive transfer of in vitro differentiated Th9 cells induces the development of autoimmune tissue inflammation in EAE and IBD. Here we describe methods for in vitro differentiation of naïve murine CD4+ T cells to generate IL-9-producing Th9 cells and follow their effector functions in EAE and IBD murine models.
Language	English
Publishing date	2017
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-6877-0_16
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