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Article ; Online: STING induces early IFN-β in the liver and constrains myeloid cell-mediated dissemination of murine cytomegalovirus.

Tegtmeyer, Pia-Katharina / Spanier, Julia / Borst, Katharina / Becker, Jennifer / Riedl, André / Hirche, Christoph / Ghita, Luca / Skerra, Jennifer / Baumann, Kira / Lienenklaus, Stefan / Doering, Marius / Ruzsics, Zsolt / Kalinke, Ulrich

Nature communications

2019 Volume 10, Issue 1, Page(s) 2830

Abstract: Cytomegalovirus is a DNA-encoded β-herpesvirus that induces STING-dependent type 1 interferon responses in macrophages and uses myeloid cells as a vehicle for dissemination. Here we report that STING knockout mice are as resistant to murine ... ...

Abstract	Cytomegalovirus is a DNA-encoded β-herpesvirus that induces STING-dependent type 1 interferon responses in macrophages and uses myeloid cells as a vehicle for dissemination. Here we report that STING knockout mice are as resistant to murine cytomegalovirus (MCMV) infection as wild-type controls, whereas mice with a combined Toll-like receptor/RIG-I-like receptor/STING signaling deficiency do not mount type 1 interferon responses and succumb to the infection. Although STING alone is dispensable for survival, early IFN-β induction in Kupffer cells is STING-dependent and controls early hepatic virus propagation. Infection experiments with an inducible reporter MCMV show that STING constrains MCMV replication in myeloid cells and limits viral dissemination via these cells. By contrast, restriction of viral dissemination from hepatocytes to other organs is independent of STING. Thus, during MCMV infection STING is involved in early IFN-β induction in Kupffer cells and the restriction of viral dissemination via myeloid cells, whereas it is dispensable for survival.
MeSH term(s)	Animals ; Female ; Hepatocytes/metabolism ; Hepatocytes/virology ; Herpesviridae Infections/veterinary ; Herpesviridae Infections/virology ; Host-Pathogen Interactions ; Interferon-beta/genetics ; Interferon-beta/metabolism ; Kupffer Cells/metabolism ; Kupffer Cells/virology ; Liver/metabolism ; Liver/virology ; Male ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Muromegalovirus/genetics ; Muromegalovirus/physiology ; Myeloid Cells/metabolism ; Myeloid Cells/virology ; Rodent Diseases/genetics ; Rodent Diseases/metabolism ; Rodent Diseases/virology ; Signal Transduction ; Toll-Like Receptors/genetics ; Toll-Like Receptors/metabolism
Chemical Substances	Membrane Proteins ; Sting1 protein, mouse ; Toll-Like Receptors ; Interferon-beta (77238-31-4)
Language	English
Publishing date	2019-06-27
Publishing country	England
Document type	Journal Article ; 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/s41467-019-10863-0
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Development of a First-in-Class Small-Molecule Inhibitor of the C-Terminal Hsp90 Dimerization.

Bhatia, Sanil / Spanier, Lukas / Bickel, David / Dienstbier, Niklas / Woloschin, Vitalij / Vogt, Melina / Pols, Henrik / Lungerich, Beate / Reiners, Jens / Aghaallaei, Narges / Diedrich, Daniela / Frieg, Benedikt / Schliehe-Diecks, Julian / Bopp, Bertan / Lang, Franziska / Gopalswamy, Mohanraj / Loschwitz, Jennifer / Bajohgli, Baubak / Skokowa, Julia /

Borkhardt, Arndt / Hauer, Julia / Hansen, Finn K / Smits, Sander H J / Jose, Joachim / Gohlke, Holger / Kurz, Thomas

ACS central science

2022 Volume 8, Issue 5, Page(s) 636–655

Abstract: Heat shock proteins 90 (Hsp90) are promising therapeutic targets due to their involvement in stabilizing several aberrantly expressed oncoproteins. In cancerous cells, Hsp90 expression is elevated, thereby exerting antiapoptotic effects, which is ... ...

Abstract	Heat shock proteins 90 (Hsp90) are promising therapeutic targets due to their involvement in stabilizing several aberrantly expressed oncoproteins. In cancerous cells, Hsp90 expression is elevated, thereby exerting antiapoptotic effects, which is essential for the malignant transformation and tumor progression. Most of the Hsp90 inhibitors (Hsp90i) under investigation target the ATP binding site in the N-terminal domain of Hsp90. However, adverse effects, including induction of the prosurvival resistance mechanism (heat shock response or HSR) and associated dose-limiting toxicity, have so far precluded their clinical approval. In contrast, modulators that interfere with the C-terminal domain (CTD) of Hsp90 do not inflict HSR. Since the CTD dimerization of Hsp90 is essential for its chaperone activity, interfering with the dimerization process by small-molecule protein-protein interaction inhibitors is a promising strategy for anticancer drug research. We have developed a first-in-class small-molecule inhibitor (
Language	English
Publishing date	2022-04-27
Publishing country	United States
Document type	Journal Article
ISSN	2374-7943
ISSN	2374-7943
DOI	10.1021/acscentsci.2c00013
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Article ; Online: Cutting Edge: Dual TCRα Expression Poses an Autoimmune Hazard by Limiting Regulatory T Cell Generation.

Schuldt, Nathaniel J / Auger, Jennifer L / Spanier, Justin A / Martinov, Tijana / Breed, Elise R / Fife, Brian T / Hogquist, Kristin A / Binstadt, Bryce A

Journal of immunology (Baltimore, Md. : 1950)

2017 Volume 199, Issue 1, Page(s) 33–38

Abstract: Despite accounting for 10-30% of the T cell population in mice and humans, the role of dual TCR-expressing T cells in immunity remains poorly understood. It has been hypothesized that dual TCR T cells pose an autoimmune hazard by allowing self-reactive ... ...

Abstract	Despite accounting for 10-30% of the T cell population in mice and humans, the role of dual TCR-expressing T cells in immunity remains poorly understood. It has been hypothesized that dual TCR T cells pose an autoimmune hazard by allowing self-reactive TCRs to escape thymic selection. We revisited this hypothesis using the NOD murine model of type 1 diabetes. We bred NOD mice hemizygous at both TCRα and β (TCRα
MeSH term(s)	Animals ; Autoimmunity ; Diabetes Mellitus, Type 1/immunology ; Mice ; Mice, Inbred NOD ; Receptors, Antigen, T-Cell, alpha-beta/genetics ; Receptors, Antigen, T-Cell, alpha-beta/immunology ; T-Lymphocytes, Regulatory/immunology ; T-Lymphocytes, Regulatory/physiology ; Thymocytes/immunology
Chemical Substances	Receptors, Antigen, T-Cell, alpha-beta
Language	English
Publishing date	2017--01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
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.1700406
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Article ; Online: STING induces early IFN-β in the liver and constrains myeloid cell-mediated dissemination of murine cytomegalovirus.

Nature communications

2019

Abstract	Cytomegalovirus is a DNA-encoded β-herpesvirus that induces STING-dependent type 1 interferon responses in macrophages and uses myeloid cells as a vehicle for dissemination. Here we report that STING knockout mice are as resistant to murine cytomegalovirus (MCMV) infection as wild-type controls, whereas mice with a combined Toll-like receptor/RIG-I-like receptor/STING signaling deficiency do not mount type 1 interferon responses and succumb to the infection. Although STING alone is dispensable for survival, early IFN-β induction in Kupffer cells is STING-dependent and controls early hepatic virus propagation. Infection experiments with an inducible reporter MCMV show that STING constrains MCMV replication in myeloid cells and limits viral dissemination via these cells. By contrast, restriction of viral dissemination from hepatocytes to other organs is independent of STING. Thus, during MCMV infection STING is involved in early IFN-β induction in Kupffer cells and the restriction of viral dissemination via myeloid cells, whereas it is dispensable for survival.
Subject code	570
Language	English
Publishing date	2019-06-27
Publisher	Springer-Nature
Publishing country	de
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: STING induces early IFN-β in the liver and constrains myeloid cell-mediated dissemination of murine cytomegalovirus.

Nature communications

2019

Abstract	Cytomegalovirus is a DNA-encoded β-herpesvirus that induces STING-dependent type 1 interferon responses in macrophages and uses myeloid cells as a vehicle for dissemination. Here we report that STING knockout mice are as resistant to murine cytomegalovirus (MCMV) infection as wild-type controls, whereas mice with a combined Toll-like receptor/RIG-I-like receptor/STING signaling deficiency do not mount type 1 interferon responses and succumb to the infection. Although STING alone is dispensable for survival, early IFN-β induction in Kupffer cells is STING-dependent and controls early hepatic virus propagation. Infection experiments with an inducible reporter MCMV show that STING constrains MCMV replication in myeloid cells and limits viral dissemination via these cells. By contrast, restriction of viral dissemination from hepatocytes to other organs is independent of STING. Thus, during MCMV infection STING is involved in early IFN-β induction in Kupffer cells and the restriction of viral dissemination via myeloid cells, whereas it is dispensable for survival.
Subject code	570
Language	English
Publishing date	2019-06-27
Publisher	Springer-Nature
Publishing country	de
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Human monocyte-derived macrophages inhibit HCMV spread independent of classical antiviral cytokines.

Becker, Jennifer / Kinast, Volker / Döring, Marius / Lipps, Christoph / Duran, Veronica / Spanier, Julia / Tegtmeyer, Pia-Katharina / Wirth, Dagmar / Cicin-Sain, Luka / Alcamí, Antonio / Kalinke, Ulrich

Virulence

2018 Volume 9, Issue 1, Page(s) 1669–1684

Abstract: Infection of healthy individuals with human cytomegalovirus (HCMV) is usually unnoticed and results in life-long latency, whereas HCMV reactivation as well as infection of newborns or immunocompromised patients can cause life-threatening disease. To ... ...

Abstract	Infection of healthy individuals with human cytomegalovirus (HCMV) is usually unnoticed and results in life-long latency, whereas HCMV reactivation as well as infection of newborns or immunocompromised patients can cause life-threatening disease. To better understand HCMV pathogenesis we studied mechanisms that restrict HCMV spread. We discovered that HCMV-infected cells can directly trigger plasmacytoid dendritic cells (pDC) to mount antiviral type I interferon (IFN-I) responses, even in the absence of cell-free virus. In contrast, monocyte-derived cells only expressed IFN-I when stimulated by cell-free HCMV, or upon encounter of HCMV-infected cells that already produced cell-free virus. Nevertheless, also in the absence of cell-free virus, i.e., upon co-culture of infected epithelial/endothelial cells and monocyte-derived macrophages (moMΦ) or dendritic cells (moDC), antiviral responses were induced that limited HCMV spread. The induction of this antiviral effect was dependent on cell-cell contact, whereas cell-free supernatants from co-culture experiments also inhibited virus spread, implying that soluble factors were critically needed. Interestingly, the antiviral effect was independent of IFN-γ, TNF-α, and IFN-I as indicated by cytokine inhibition experiments using neutralizing antibodies or the vaccinia virus-derived soluble IFN-I binding protein B18R, which traps human IFN-α and IFN-β. In conclusion, our results indicate that human macrophages and dendritic cells can limit HCMV spread by IFN-I dependent as well as independent mechanisms, whereas the latter ones might be particularly relevant for the restriction of HCMV transmission via cell-to-cell spread.
MeSH term(s)	Antibodies, Neutralizing/immunology ; Coculture Techniques ; Culture Media ; Cytokines/antagonists & inhibitors ; Cytokines/immunology ; Cytomegalovirus ; Epithelial Cells/drug effects ; Epithelial Cells/virology ; Humans ; Interferon Type I/immunology ; Interferon-beta/immunology ; Macrophages/immunology ; Macrophages/virology ; Tumor Necrosis Factor-alpha/immunology ; Virus Replication/drug effects
Chemical Substances	Antibodies, Neutralizing ; Culture Media ; Cytokines ; Interferon Type I ; Tumor Necrosis Factor-alpha ; Interferon-beta (77238-31-4)
Language	English
Publishing date	2018-11-29
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2657572-3
ISSN	2150-5608 ; 2150-5594
ISSN (online)	2150-5608
ISSN	2150-5594
DOI	10.1080/21505594.2018.1535785
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Article: Development of perturbation Monte Carlo methods for polarized light transport in a discrete particle scattering model.

Nguyen, Jennifer / Hayakawa, Carole K / Mourant, Judith R / Venugopalan, Vasan / Spanier, Jerome

Biomedical optics express

2016 Volume 7, Issue 5, Page(s) 2051–2066

Abstract: We present a polarization-sensitive, transport-rigorous perturbation Monte Carlo (pMC) method to model the impact of optical property changes on reflectance measurements within a discrete particle scattering model. The model consists of three log- ... ...

Abstract	We present a polarization-sensitive, transport-rigorous perturbation Monte Carlo (pMC) method to model the impact of optical property changes on reflectance measurements within a discrete particle scattering model. The model consists of three log-normally distributed populations of Mie scatterers that approximate biologically relevant cervical tissue properties. Our method provides reflectance estimates for perturbations across wavelength and/or scattering model parameters. We test our pMC model performance by perturbing across number densities and mean particle radii, and compare pMC reflectance estimates with those obtained from conventional Monte Carlo simulations. These tests allow us to explore different factors that control pMC performance and to evaluate the gains in computational efficiency that our pMC method provides.
Language	English
Publishing date	2016-04-28
Publishing country	United States
Document type	Journal Article
ZDB-ID	2572216-5
ISSN	2156-7085
ISSN	2156-7085
DOI	10.1364/BOE.7.002051
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Article: A systematic review of alternative therapies in the irritable bowel syndrome.

Spanier, Jennifer A / Howden, Colin W / Jones, Michael P

Archives of internal medicine

2003 Volume 163, Issue 3, Page(s) 265–274

Abstract: The irritable bowel syndrome is a common disorder associated with a significant burden of illness, poor quality of life, high rates of absenteeism, and high health care utilization. Management can be difficult and treatment unrewarding; these facts have ... ...

Abstract	The irritable bowel syndrome is a common disorder associated with a significant burden of illness, poor quality of life, high rates of absenteeism, and high health care utilization. Management can be difficult and treatment unrewarding; these facts have led physicians and patients toward alternative therapies. We explored a variety of treatments that exist beyond the scope of commonly used therapies for irritable bowel syndrome. Guarded optimism exists for traditional Chinese medicine and psychological therapies, but further well-designed trials are needed. Oral cromolyn sodium may be useful in chronic unexplained diarrhea and appears as effective as and safer than elimination diets. The roles of lactose and fructose intolerance remain poorly understood. Alterations of enteric flora may play a role in irritable bowel syndrome, but supporting evidence for bacterial overgrowth or probiotic therapy is lacking.
MeSH term(s)	Behavior Therapy ; Colonic Diseases, Functional/diet therapy ; Colonic Diseases, Functional/etiology ; Colonic Diseases, Functional/microbiology ; Colonic Diseases, Functional/psychology ; Colonic Diseases, Functional/therapy ; Combined Modality Therapy ; Complementary Therapies ; Cromolyn Sodium/therapeutic use ; Dietary Supplements ; Food Hypersensitivity/complications ; Food Hypersensitivity/diet therapy ; Humans ; Hypnosis ; Meta-Analysis as Topic ; Plant Preparations/therapeutic use ; Psychotherapy
Chemical Substances	Plant Preparations ; Cromolyn Sodium (Q2WXR1I0PK)
Language	English
Publishing date	2003-02-10
Publishing country	United States
Document type	Journal Article ; Review ; Systematic Review
ZDB-ID	211575-x
ISSN	1538-3679 ; 0003-9926 ; 0888-2479 ; 0730-188X
ISSN (online)	1538-3679
ISSN	0003-9926 ; 0888-2479 ; 0730-188X
DOI	10.1001/archinte.163.3.265
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Article ; Online: Human monocyte-derived macrophages inhibit HCMV spread independent of classical antiviral cytokines.

Virulence

2018

Abstract	Infection of healthy individuals with human cytomegalovirus (HCMV) is usually unnoticed and results in life-long latency, whereas HCMV reactivation as well as infection of newborns or immunocompromised patients can cause life-threatening disease. To better understand HCMV pathogenesis we studied mechanisms that restrict HCMV spread. We discovered that HCMV-infected cells can directly trigger plasmacytoid dendritic cells (pDC) to mount antiviral type I interferon (IFN-I) responses, even in the absence of cell-free virus. In contrast, monocyte-derived cells only expressed IFN-I when stimulated by cell-free HCMV, or upon encounter of HCMV-infected cells that already produced cell-free virus. Nevertheless, also in the absence of cell-free virus, i.e., upon co-culture of infected epithelial/endothelial cells and monocyte-derived macrophages (moMΦ) or dendritic cells (moDC), antiviral responses were induced that limited HCMV spread. The induction of this antiviral effect was dependent on cell-cell contact, whereas cell-free supernatants from co-culture experiments also inhibited virus spread, implying that soluble factors were critically needed. Interestingly, the antiviral effect was independent of IFN-γ, TNF-α, and IFN-I as indicated by cytokine inhibition experiments using neutralizing antibodies or the vaccinia virus-derived soluble IFN-I binding protein B18R, which traps human IFN-α and IFN-β. In conclusion, our results indicate that human macrophages and dendritic cells can limit HCMV spread by IFN-I dependent as well as independent mechanisms, whereas the latter ones might be particularly relevant for the restriction of HCMV transmission via cell-to-cell spread.
Keywords	Human cytomegalovirus ; epithelial cells ; macrophages ; plasmacytoid dendritic cells ; type I interferons
Subject code	610 ; 570
Publishing date	2018-01-01
Publishing country	de
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Human monocyte-derived macrophages inhibit HCMV spread independent of classical antiviral cytokines.

Virulence

2018

Abstract	Infection of healthy individuals with human cytomegalovirus (HCMV) is usually unnoticed and results in life-long latency, whereas HCMV reactivation as well as infection of newborns or immunocompromised patients can cause life-threatening disease. To better understand HCMV pathogenesis we studied mechanisms that restrict HCMV spread. We discovered that HCMV-infected cells can directly trigger plasmacytoid dendritic cells (pDC) to mount antiviral type I interferon (IFN-I) responses, even in the absence of cell-free virus. In contrast, monocyte-derived cells only expressed IFN-I when stimulated by cell-free HCMV, or upon encounter of HCMV-infected cells that already produced cell-free virus. Nevertheless, also in the absence of cell-free virus, i.e., upon co-culture of infected epithelial/endothelial cells and monocyte-derived macrophages (moMΦ) or dendritic cells (moDC), antiviral responses were induced that limited HCMV spread. The induction of this antiviral effect was dependent on cell-cell contact, whereas cell-free supernatants from co-culture experiments also inhibited virus spread, implying that soluble factors were critically needed. Interestingly, the antiviral effect was independent of IFN-γ, TNF-α, and IFN-I as indicated by cytokine inhibition experiments using neutralizing antibodies or the vaccinia virus-derived soluble IFN-I binding protein B18R, which traps human IFN-α and IFN-β. In conclusion, our results indicate that human macrophages and dendritic cells can limit HCMV spread by IFN-I dependent as well as independent mechanisms, whereas the latter ones might be particularly relevant for the restriction of HCMV transmission via cell-to-cell spread.
Keywords	Human cytomegalovirus ; epithelial cells ; macrophages ; plasmacytoid dendritic cells ; type I interferons
Subject code	610 ; 570
Publishing date	2018-01-01
Publishing country	de
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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