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Article ; Online: Reply to: "Hepatocyte expression of hepatitis B surface and core antigens across phases of chronic hepatitis B infection".

Aggarwal, Abhishek / Montanari, Noe Rico / Ramírez, Ricardo / Diehl, Lauri / Feierbach, Becket / Boonstra, Andre

2022 Volume 77, Issue 5, Page(s) 1457

MeSH term(s)	Hepatitis B ; Hepatitis B Core Antigens ; Hepatitis B Surface Antigens ; Hepatitis B e Antigens ; Hepatitis B virus ; Hepatitis B, Chronic ; Hepatocytes/metabolism ; Humans ; Liver/metabolism
Chemical Substances	Hepatitis B Core Antigens ; Hepatitis B Surface Antigens ; Hepatitis B e Antigens
Language	English
Publishing date	2022-08-14
Publishing country	Netherlands
Document type	Letter ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	605953-3
ISSN	1600-0641 ; 0168-8278
ISSN (online)	1600-0641
ISSN	0168-8278
DOI	10.1016/j.jhep.2022.07.033
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Article ; Online: Multi-parametric analysis of human livers reveals variation in intrahepatic inflammation across phases of chronic hepatitis B infection.

Montanari, Noe Rico / Ramírez, Ricardo / Aggarwal, Abhishek / van Buuren, Nick / Doukas, Michael / Moon, Christina / Turner, Scott / Diehl, Lauri / Li, Li / Debes, Jose D / Feierbach, Becket / Boonstra, Andre

Journal of hepatology

2022 Volume 77, Issue 2, Page(s) 332–343

Abstract: Background & aims: Chronic HBV is clinically categorized into 4 phases by a combination of serum HBV DNA levels, HBeAg status and alanine aminotransferase (ALT): immunotolerant (IT), immune-active (IA), inactive carrier (IC) and HBeAg-negative hepatitis ...

Abstract	Background & aims: Chronic HBV is clinically categorized into 4 phases by a combination of serum HBV DNA levels, HBeAg status and alanine aminotransferase (ALT): immunotolerant (IT), immune-active (IA), inactive carrier (IC) and HBeAg-negative hepatitis (ENEG). Immune and virological measurements in the blood have proven useful but are insufficient to explain the interrelation between the immune system and the virus since immune dynamics differ in the blood and liver. Furthermore, the inflammatory response in the liver and parenchymal cells cannot be fully captured in blood. Methods: Immunological composition and transcriptional profiles of core needle liver-biopsies in chronic HBV phases were compared to those of healthy controls by multiplex immunofluorescence and RNA-sequencing (n = 37 and 78, respectively) analyses. Results: Irrespective of the phase-specific serological profiles, increased immune-gene expression and frequency was observed in chronic HBV compared to healthy livers. Greater transcriptomic deregulation was seen in IA and ENEG (172 vs. 243 DEGs) than in IT and IC (13 vs. 35 DEGs) livers. Interferon-stimulated genes, immune-activation and exhaustion genes (ICOS, CTLA4, PDCD1) together with chemokine genes (CXCL10, CXCL9) were significantly induced in IA and ENEG livers. Moreover, distinct immune profiles associated with ALT elevation and a more accentuated immune-exhaustion profile (CTLA4, TOX, SLAMF6, FOXP3) were observed in ENEG, which set it apart from the IA phase (LGALS9, PDCD1). Interestingly, all HBV phases showed downregulation of metabolic pathways vs. healthy livers (fatty and bile acid metabolism). Finally, increased leukocyte infiltrate correlated with serum ALT, but not with HBV DNA or viral proteins. Conclusion: Our comprehensive multi-parametric analysis of human livers revealed distinct inflammatory profiles and pronounced differences in intrahepatic gene profiles across all chronic HBV phases in comparison to healthy liver. Lay summary: Immunological studies on chronic HBV remain largely restricted to assessment of peripheral responses due to the limited access to the site of infection, the liver. In this study, we comprehensively analyzed livers from a well-defined cohort of patients with chronic HBV and uninfected controls with state-of-the-art techniques, and evaluated the differences in gene expression profiles and inflammation characteristics across distinct disease phases in patients with chronic HBV.
MeSH term(s)	CTLA-4 Antigen ; DNA, Viral/genetics ; Hepatitis B ; Hepatitis B e Antigens ; Hepatitis B virus/genetics ; Hepatitis B, Chronic ; Humans ; Inflammation/genetics
Chemical Substances	CTLA-4 Antigen ; DNA, Viral ; Hepatitis B e Antigens
Language	English
Publishing date	2022-02-24
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	605953-3
ISSN	1600-0641 ; 0168-8278
ISSN (online)	1600-0641
ISSN	0168-8278
DOI	10.1016/j.jhep.2022.02.016
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Article ; Online: Intrahepatic quantification of HBV antigens in chronic hepatitis B reveals heterogeneity and treatment-mediated reductions in HBV core-positive cells.

Aggarwal, Abhishek / Odorizzi, Pamela M / Brodbeck, Jens / van Buuren, Nicholas / Moon, Christina / Chang, Silvia / Adona, MaryVic / Suthram, Silpa / Suri, Vithika / Trowe, Torsten / Turner, Scott / Marcellin, Patrick / Buti, Maria / Gaggar, Anuj / Fletcher, Simon P / Diehl, Lauri / Feierbach, Becket / Balsitis, Scott

JHEP reports : innovation in hepatology

2022 Volume 5, Issue 4, Page(s) 100664

Abstract: ... with chronic hepatitis B and evaluated sampling heterogeneity, effects of disease stage, and nucleos(t)ide (NUC ... were compared. Serum or plasma samples were evaluated for levels of HBV DNA, HBsAg, hepatitis B core ...

Abstract	Background & aims: Patterns of liver HBV antigen expression have been described but not quantified at single-cell resolution. We applied quantitative techniques to liver biopsies from individuals with chronic hepatitis B and evaluated sampling heterogeneity, effects of disease stage, and nucleos(t)ide (NUC) treatment, and correlations between liver and peripheral viral biomarkers. Methods: Hepatocytes positive for HBV core and HBsAg were quantified using a novel four-plex immunofluorescence assay and image analysis. Biopsies were analysed from HBeAg-positive (n = 39) and HBeAg-negative (n = 75) participants before and after NUC treatment. To evaluate sampling effects, duplicate biopsies collected at the same time point were compared. Serum or plasma samples were evaluated for levels of HBV DNA, HBsAg, hepatitis B core-related antigen (HBcrAg), and HBV RNA. Results: Diffusely distributed individual HBV core+ cells and foci of HBsAg+ cells were the most common staining patterns. Hepatocytes positive for both HBV core and HBsAg were rare. Paired biopsies revealed large local variation in HBV staining within participants, which was confirmed in a large liver resection. NUC treatment was associated with a >100-fold lower median frequency of HBV core+ cells in HBeAg-positive and HBeAg-negative participants, whereas reductions in HBsAg+ cells were not statistically significant. The frequency of HBV core+ hepatocytes was lower in HBeAg-negative participants than in HBeAg-positive participants at all time points evaluated. Total HBV+ hepatocyte burden correlated with HBcrAg, HBV DNA, and HBV RNA only in baseline HBeAg-positive samples. Conclusions: Reductions in HBV core+ hepatocytes were associated with HBeAg-negative status and NUC treatment. Variation in HBV positivity within individual livers was extensive. Correlations between the liver and the periphery were found only between biomarkers likely indicative of cccDNA (HBV core+ and HBcrAg, HBV DNA, and RNA). Impact and implications: HBV infects liver hepatocyte cells, and its genome can exist in two forms that express different sets of viral proteins: a circular genome called cccDNA that can express all viral proteins, including the HBV core and HBsAg proteins, or a linear fragment that inserts into the host genome typically to express HBsAg, but not HBV core. We used new techniques to determine the percentage of hepatocytes expressing the HBV core and HBsAg proteins in a large set of liver biopsies. We find that abundance and patterns of expression differ across patient groups and even within a single liver and that NUC treatment greatly reduces the number of core-expressing hepatocytes.
Language	English
Publishing date	2022-12-26
Publishing country	Netherlands
Document type	Journal Article
ISSN	2589-5559
ISSN (online)	2589-5559
DOI	10.1016/j.jhepr.2022.100664
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Article ; Online: c-Rel gain in B cells drives germinal center reactions and autoantibody production.

Kober-Hasslacher, Maike / Oh-Strauß, Hyunju / Kumar, Dilip / Soberon, Valeria / Diehl, Carina / Lech, Maciej / Engleitner, Thomas / Katab, Eslam / Fernández-Sáiz, Vanesa / Piontek, Guido / Li, Hongwei / Menze, Björn / Ziegenhain, Christoph / Enard, Wolfgang / Rad, Roland / Böttcher, Jan P / Anders, Hans-Joachim / Rudelius, Martina / Schmidt-Supprian, Marc

The Journal of clinical investigation

2020 Volume 130, Issue 6, Page(s) 3270–3286

Abstract: ... to human autoimmune diseases and B cell lymphomas, respectively. However, the functional consequences ... of enhanced c-Rel levels remain enigmatic. Here, we overexpressed c-Rel specifically in mouse B cells from BAC ... B (GCB) cells and isotype-switched plasma cells. c-Rel expression in B cells of otherwise c-Rel ...

Abstract	Single-nucleotide polymorphisms and locus amplification link the NF-κB transcription factor c-Rel to human autoimmune diseases and B cell lymphomas, respectively. However, the functional consequences of enhanced c-Rel levels remain enigmatic. Here, we overexpressed c-Rel specifically in mouse B cells from BAC-transgenic gene loci and demonstrate that c-Rel protein levels linearly dictated expansion of germinal center B (GCB) cells and isotype-switched plasma cells. c-Rel expression in B cells of otherwise c-Rel-deficient mice fully rescued terminal B cell differentiation, underscoring its critical B cell-intrinsic roles. Unexpectedly, in GCB cells transcription-independent regulation produced the highest c-Rel protein levels among B cell subsets. In c-Rel-overexpressing GCB cells this caused enhanced nuclear translocation, a profoundly altered transcriptional program, and increased proliferation. Finally, we provide a link between c-Rel gain and autoimmunity by showing that c-Rel overexpression in B cells caused autoantibody production and renal immune complex deposition.
MeSH term(s)	Animals ; Antibody Formation ; Autoantibodies/genetics ; Autoantibodies/immunology ; Germinal Center/immunology ; Germinal Center/pathology ; Mice ; Mice, Transgenic ; Plasma Cells/immunology ; Plasma Cells/pathology ; Polymorphism, Single Nucleotide ; Proto-Oncogene Proteins c-rel/genetics ; Proto-Oncogene Proteins c-rel/immunology
Chemical Substances	Autoantibodies ; Proto-Oncogene Proteins c-rel
Language	English
Publishing date	2020-03-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI124382
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Article ; Online: Infant antibody and B-cell responses following confirmed pediatric GII.17 norovirus infections functionally distinguish GII.17 genetic clusters.

Strother, Camilla A / Brewer-Jensen, Paul D / Becker-Dreps, Sylvia / Zepeda, Omar / May, Samantha / Gonzalez, Fredman / Reyes, Yaoska / McElvany, Benjamin D / Averill, April M / Mallory, Michael L / Montmayeur, Anna M / Costantini, Verónica P / Vinjé, Jan / Baric, Ralph S / Bucardo, Filemon / Lindesmith, Lisa C / Diehl, Sean A

Frontiers in immunology

2023 Volume 14, Page(s) 1229724

Abstract: ... from a birth cohort, we investigated antibody and B-cell responses to GII.17 cluster variants in confirmed GII ... in a surrogate virus neutralization assay. Antibodies secreted by immortalized memory B cells (MBCs ...

Abstract	Genogroup II (GII) noroviruses are a major cause of diarrheal disease burden in children in both high- and low-income countries. GII.17 noroviruses are composed of distinct genetic clusters (I, II, IIIa, and IIIb) and have shown potential for replacing historically more prevalent GII.4 strains, but the serological basis for GII.17 antigenic diversity has not been studied in children. Utilizing samples from a birth cohort, we investigated antibody and B-cell responses to GII.17 cluster variants in confirmed GII.17 infections in young children as well as demonstrated that the distinct genetic clusters co-circulate. Polyclonal serum antibodies bound multiple clusters but showed cluster-specific blockade activity in a surrogate virus neutralization assay. Antibodies secreted by immortalized memory B cells (MBCs) from an infant GII.17 case were highly specific to GII.17 and exhibited blockade activity against this genotype. We isolated an MBC-derived GII.17-specific Immunoglobulin A (IgA) monoclonal antibody called NVA.1 that potently and selectively blocked GII.17 cluster IIIb and recognized an epitope targeted in serum from cluster IIIb-infected children. These data indicate that multiple antigenically distinct GII.17 variants co-circulate in young children, suggesting retention of cluster diversity alongside potential for immune escape given the existence of antibody-defined cluster-specific epitopes elicited during infection.
MeSH term(s)	Child ; Infant ; Humans ; Child, Preschool ; B-Lymphocytes ; Antibodies, Monoclonal ; Memory B Cells ; Immunoglobulin A ; Paraproteins ; Epitopes ; Genotype ; Norovirus/genetics
Chemical Substances	Antibodies, Monoclonal ; Immunoglobulin A ; Paraproteins ; Epitopes
Language	English
Publishing date	2023-08-18
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2023.1229724
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Article ; Online: Evidence for a B_{s}^{0}π^{±} State.

Abazov, V M / Abbott, B / Acharya, B S / Adams, M / Adams, T / Agnew, J P / Alexeev, G D / Alkhazov, G / Alton, A / Askew, A / Atkins, S / Augsten, K / Aushev, V / Aushev, Y / Avila, C / Badaud, F / Bagby, L / Baldin, B / Bandurin, D V /

Banerjee, S / Barberis, E / Baringer, P / Bartlett, J F / Bassler, U / Bazterra, V / Bean, A / Begalli, M / Bellantoni, L / Beri, S B / Bernardi, G / Bernhard, R / Bertram, I / Besançon, M / Beuselinck, R / Bhat, P C / Bhatia, S / Bhatnagar, V / Blazey, G / Blessing, S / Bloom, K / Boehnlein, A / Boline, D / Boos, E E / Borissov, G / Borysova, M / Brandt, A / Brandt, O / Brochmann, M / Brock, R / Bross, A / Brown, D / Bu, X B / Buehler, M / Buescher, V / Bunichev, V / Burdin, S / Buszello, C P / Camacho-Pérez, E / Casey, B C K / Castilla-Valdez, H / Caughron, S / Chakrabarti, S / Chan, K M / Chandra, A / Chapon, E / Chen, G / Cho, S W / Choi, S / Choudhary, B / Cihangir, S / Claes, D / Clutter, J / Cooke, M / Cooper, W E / Corcoran, M / Couderc, F / Cousinou, M-C / Cuth, J / Cutts, D / Das, A / Davies, G / de Jong, S J / De La Cruz-Burelo, E / Déliot, F / Demina, R / Denisov, D / Denisov, S P / Desai, S / Deterre, C / DeVaughan, K / Diehl, H T / Diesburg, M / Ding, P F / Dominguez, A / Drutskoy, A / Dubey, A / Dudko, L V / Duperrin, A / Dutt, S / Eads, M / Edmunds, D / Ellison, J / Elvira, V D / Enari, Y / Evans, H / Evdokimov, A / Evdokimov, V N / Fauré, A / Feng, L / Ferbel, T / Fiedler, F / Filthaut, F / Fisher, W / Fisk, H E / Fortner, M / Fox, H / Franc, J / Fuess, S / Garbincius, P H / Garcia-Bellido, A / García-González, J A / Gavrilov, V / Geng, W / Gerber, C E / Gershtein, Y / Ginther, G / Gogota, O / Golovanov, G / Grannis, P D / Greder, S / Greenlee, H / Grenier, G / Gris, Ph / Grivaz, J-F / Grohsjean, A / Grünendahl, S / Grünewald, M W / Guillemin, T / Gutierrez, G / Gutierrez, P / Haley, J / Han, L / Harder, K / Harel, A / Hauptman, J M / Hays, J / Head, T / Hebbeker, T / Hedin, D / Hegab, H / Heinson, A P / Heintz, U / Hensel, C / Heredia-De La Cruz, I / Herner, K / Hesketh, G / Hildreth, M D / Hirosky, R / Hoang, T / Hobbs, J D / Hoeneisen, B / Hogan, J / Hohlfeld, M / Holzbauer, J L / Howley, I / Hubacek, Z / Hynek, V / Iashvili, I / Ilchenko, Y / Illingworth, R / Ito, A S / Jabeen, S / Jaffré, M / Jayasinghe, A / Jeong, M S / Jesik, R / Jiang, P / Johns, K / Johnson, E / Johnson, M / Jonckheere, A / Jonsson, P / Joshi, J / Jung, A W / Juste, A / Kajfasz, E / Karmanov, D / Katsanos, I / Kaur, M / Kehoe, R / Kermiche, S / Khalatyan, N / Khanov, A / Kharchilava, A / Kharzheev, Y N / Kiselevich, I / Kohli, J M / Kozelov, A V / Kraus, J / Kumar, A / Kupco, A / Kurča, T / Kuzmin, V A / Lammers, S / Lebrun, P / Lee, H S / Lee, S W / Lee, W M / Lei, X / Lellouch, J / Li, D / Li, H / Li, L / Li, Q Z / Lim, J K / Lincoln, D / Linnemann, J / Lipaev, V V / Lipton, R / Liu, H / Liu, Y / Lobodenko, A / Lokajicek, M / Lopes de Sa, R / Luna-Garcia, R / Lyon, A L / Maciel, A K A / Madar, R / Magaña-Villalba, R / Malik, S / Malyshev, V L / Mansour, J / Martínez-Ortega, J / McCarthy, R / McGivern, C L / Meijer, M M / Melnitchouk, A / Menezes, D / Mercadante, P G / Merkin, M / Meyer, A / Meyer, J / Miconi, F / Mondal, N K / Mulhearn, M / Nagy, E / Narain, M / Nayyar, R / Neal, H A / Negret, J P / Neustroev, P / Nguyen, H T / Nunnemann, T / Orduna, J / Osman, N / Pal, A / Parashar, N / Parihar, V / Park, S K / Partridge, R / Parua, N / Patwa, A / Penning, B / Perfilov, M / Peters, Y / Petridis, K / Petrillo, G / Pétroff, P / Pleier, M-A / Podstavkov, V M / Popov, A V / Prewitt, M / Price, D / Prokopenko, N / Qian, J / Quadt, A / Quinn, B / Ratoff, P N / Razumov, I / Ripp-Baudot, I / Rizatdinova, F / Rominsky, M / Ross, A / Royon, C / Rubinov, P / Ruchti, R / Sajot, G / Sánchez-Hernández, A / Sanders, M P / Santos, A S / Savage, G / Savitskyi, M / Sawyer, L / Scanlon, T / Schamberger, R D / Scheglov, Y / Schellman, H / Schott, M / Schwanenberger, C / Schwienhorst, R / Sekaric, J / Severini, H / Shabalina, E / Shary, V / Shaw, S / Shchukin, A A / Simak, V / Skubic, P / Slattery, P / Snow, G R / Snow, J / Snyder, S / Söldner-Rembold, S / Sonnenschein, L / Soustruznik, K / Stark, J / Stefaniuk, N / Stoyanova, D A / Strauss, M / Suter, L / Svoisky, P / Titov, M / Tokmenin, V V / Tsai, Y-T / Tsybychev, D / Tuchming, B / Tully, C / Uvarov, L / Uvarov, S / Uzunyan, S / Van Kooten, R / van Leeuwen, W M / Varelas, N / Varnes, E W / Vasilyev, I A / Verkheev, A Y / Vertogradov, L S / Verzocchi, M / Vesterinen, M / Vilanova, D / Vokac, P / Wahl, H D / Wang, M H L S / Warchol, J / Watts, G / Wayne, M / Weichert, J / Welty-Rieger, L / Williams, M R J / Wilson, G W / Wobisch, M / Wood, D R / Wyatt, T R / Xie, Y / Yamada, R / Yang, S / Yasuda, T / Yatsunenko, Y A / Ye, W / Ye, Z / Yin, H / Yip, K / Youn, S W / Yu, J M / Zennamo, J / Zhao, T G / Zhou, B / Zhu, J / Zielinski, M / Zieminska, D / Zivkovic, L

Physical review letters

2016 Volume 117, Issue 2, Page(s) 22003

Abstract: We report evidence for a narrow structure, X(5568), in the decay sequence X(5568)→B_{s}^{0}π^{±}, B ... shifted up by m(B_{s}^{*})-m(B_{s}^{0})∼49 MeV/c^{2}. This measurement is based on 10.4 fb^{-1} of pp ... MeV/c^{2}. If the decay is X(5568)→B_{s}^{*}π^{±}→B_{s}^{0}γπ^{±} with an unseen γ, m(X(5568)) will be ...

Abstract	We report evidence for a narrow structure, X(5568), in the decay sequence X(5568)→B_{s}^{0}π^{±}, B_{s}^{0}→J/ψϕ, J/ψ→μ^{+}μ^{-}, ϕ→K^{+}K^{-}. This is evidence for the first instance of a hadronic state with valence quarks of four different flavors. The mass and natural width of this state are measured to be m=5567.8±2.9(stat)_{-1.9}^{+0.9}(syst) MeV/c^{2} and Γ=21.9±6.4(stat)_{-2.5}^{+5.0}(syst) MeV/c^{2}. If the decay is X(5568)→B_{s}^{}π^{±}→B_{s}^{0}γπ^{±} with an unseen γ, m(X(5568)) will be shifted up by m(B_{s}^{})-m(B_{s}^{0})∼49 MeV/c^{2}. This measurement is based on 10.4 fb^{-1} of pp[over ¯] collision data at sqrt[s]=1.96 TeV collected by the D0 experiment at the Fermilab Tevatron collider.
Language	English
Publishing date	2016-07-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	208853-8
ISSN	1079-7114 ; 0031-9007
ISSN (online)	1079-7114
ISSN	0031-9007
DOI	10.1103/PhysRevLett.117.022003
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Article ; Online: Longitudinal analysis of acute and convalescent B cell responses in a human primary dengue serotype 2 infection model.

Nivarthi, Usha K / Tu, Huy A / Delacruz, Matthew J / Swanstrom, Jesica / Patel, Bhumi / Durbin, Anna P / Whitehead, Stephen S / Pierce, Kristen K / Kirkpatrick, Beth D / Baric, Ralph S / Nguyen, Ngan / Emerling, Daniel E / de Silva, Aravinda M / Diehl, Sean A

EBioMedicine

2019 Volume 41, Page(s) 465–478

Abstract: ... plasmablasts. At convalescence, memory B cells (MBC) and long-lived plasma cells (LLPC) are responsible ... relationships between antibodies produced by these B cell compartments are poorly understood.: Methods ... acute and convalescent B-cell responses.: Findings: The level of DENV2 replication was correlated ...

Abstract	Background: Acute viral infections induce a rapid and transient increase in antibody-secreting plasmablasts. At convalescence, memory B cells (MBC) and long-lived plasma cells (LLPC) are responsible for long-term humoral immunity. Following an acute viral infection, the specific properties and relationships between antibodies produced by these B cell compartments are poorly understood. Methods: We utilized a controlled human challenge model of primary dengue virus serotype 2 (DENV2) infection to study acute and convalescent B-cell responses. Findings: The level of DENV2 replication was correlated with the magnitude of the plasmablast response. Functional analysis of plasmablast-derived monoclonal antibodies showed that the DENV2-specific response was dominated by cells producing DENV2 serotype-specific antibodies. DENV2-neutralizing antibodies targeted quaternary structure epitopes centered on domain III of the viral envelope protein (EDIII). Functional analysis of MBC and serum antibodies from the same subjects six months post-challenge revealed maintenance of the serotype-specific response in both compartments. The serum response mainly targeted DENV2 serotype-specific epitopes on EDIII. Interpretation: Our data suggest overall functional alignment of DENV2-specific responses from the plasmablast, through the MBC and LLPC compartments following primary DENV2 inflection. These results provide enhanced resolution of the temporal and specificity of the B cell compartment in viral infection and serve as framework for evaluation of B cell responses in challenge models. Funding: This study was supported by the Bill and Melinda Gates Foundation and the National Institutes of Health.
MeSH term(s)	Acute Disease ; Antibodies, Neutralizing/blood ; Antibodies, Neutralizing/immunology ; B-Lymphocytes/cytology ; B-Lymphocytes/immunology ; B-Lymphocytes/metabolism ; Dengue/diagnosis ; Dengue/virology ; Dengue Virus/genetics ; Dengue Virus/isolation & purification ; Epitope Mapping ; Epitopes/immunology ; Humans ; Leukocytes, Mononuclear/cytology ; Leukocytes, Mononuclear/virology ; Longitudinal Studies ; Plasma Cells/cytology ; Plasma Cells/metabolism ; Serogroup ; Viral Envelope Proteins/immunology
Chemical Substances	Antibodies, Neutralizing ; Epitopes ; Viral Envelope Proteins
Language	English
Publishing date	2019-03-08
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2851331-9
ISSN	2352-3964
ISSN (online)	2352-3964
DOI	10.1016/j.ebiom.2019.02.060
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Article ; Online: Phase I Study of the Combination of Bendamustine, Rituximab, and Pixantrone in Patients With Relapsed/Refractory B-cell Non-Hodgkin Lymphoma.

Heyman, Benjamin / Rizzieri, David / Adams, David J / De Castro, Carlos / Diehl, Louis / Li, Zhiguo / Moore, Joseph / Beaven, Anne

Clinical lymphoma, myeloma & leukemia

2018 Volume 18, Issue 10, Page(s) 679–686

Abstract: ... with relapsed/refractory (R/R) aggressive B-cell non-Hodgkin lymphoma (NHL).: Patients and methods: Eligible ... patients included adults with biopsy-proven R/R B-cell NHL who met the criteria for treatment. Patients ... of pixantrone of 115 mg/m: Conclusion: The BuRP regimen was found to be safe in patients with R/R B-cell NHL ...

Abstract	Background: For patients with aggressive lymphomas who relapse after initial therapy, a durable response is rarely achieved with standard salvage therapies. Significant efforts have focused on the development of novel treatments with reduced toxicity. We conducted a phase I prospective single arm clinical trial of the novel combination of BuRP (bendamustine, rituximab, and pixantrone) in patients with relapsed/refractory (R/R) aggressive B-cell non-Hodgkin lymphoma (NHL). Patients and methods: Eligible patients included adults with biopsy-proven R/R B-cell NHL who met the criteria for treatment. Patients received bendamustine 120 mg/m Results: Twenty-two patients were enrolled onto the study with a median follow-up of 7.9 months. The maximum tolerated dose was not reached, but the highest dose level of pixantrone of 115 mg/m Conclusion: The BuRP regimen was found to be safe in patients with R/R B-cell NHL. The favorable toxicity profile plus the encouraging response rates seen suggest that continued investigation of the highest dose level is warranted.
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Bendamustine Hydrochloride/administration & dosage ; Drug Resistance, Neoplasm/drug effects ; Female ; Follow-Up Studies ; Humans ; Isoquinolines/administration & dosage ; Lymphoma, B-Cell/drug therapy ; Lymphoma, B-Cell/pathology ; Male ; Maximum Tolerated Dose ; Middle Aged ; Neoplasm Recurrence, Local/drug therapy ; Neoplasm Recurrence, Local/pathology ; Prognosis ; Prospective Studies ; Rituximab/administration & dosage ; Salvage Therapy ; Survival Rate
Chemical Substances	Isoquinolines ; Rituximab (4F4X42SYQ6) ; Bendamustine Hydrochloride (981Y8SX18M) ; pixantrone (F5SXN2KNMR)
Language	English
Publishing date	2018-07-29
Publishing country	United States
Document type	Clinical Trial, Phase I ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2540992-X
ISSN	2152-2669 ; 2152-2650
ISSN (online)	2152-2669
ISSN	2152-2650
DOI	10.1016/j.clml.2018.07.285
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Article ; Online: Massively Parallel Sequencing of Peritoneal and Splenic B Cell Repertoires Highlights Unique Properties of B-1 Cell Antibodies.

Prohaska, Thomas A / Que, Xuchu / Diehl, Cody J / Hendrikx, Sabrina / Chang, Max W / Jepsen, Kristen / Glass, Christopher K / Benner, Christopher / Witztum, Joseph L

Journal of immunology (Baltimore, Md. : 1950)

2018 Volume 200, Issue 5, Page(s) 1702–1717

Abstract: B-1 cells are a unique subset of B cells that are positively selected for expressing autoreactive ... BCRs. We isolated RNA from peritoneal (B-1a, B-1b, B-2) and splenic (B-1a, marginal zone, follicular ... B cells from C57BL/6 mice and used 5'-RACE to amplify the IgH V region using massively parallel sequencing ...

Abstract	B-1 cells are a unique subset of B cells that are positively selected for expressing autoreactive BCRs. We isolated RNA from peritoneal (B-1a, B-1b, B-2) and splenic (B-1a, marginal zone, follicular) B cells from C57BL/6 mice and used 5'-RACE to amplify the IgH V region using massively parallel sequencing. By analyzing 379,000 functional transcripts, we demonstrate that B-1a cells use a distinct and restricted repertoire. All B-1 cell subsets, especially peritoneal B-1a cells, had a high proportion of sequences without N additions, suggesting predominantly prenatal development. Their transcripts differed markedly and uniquely contained V
MeSH term(s)	Amino Acid Sequence ; Animals ; Antibodies/genetics ; Antibodies/immunology ; Antibody Diversity/genetics ; Antibody Diversity/immunology ; B-Lymphocyte Subsets/immunology ; Base Sequence ; Female ; Genes, Immunoglobulin/genetics ; Genes, Immunoglobulin/immunology ; Immunoglobulin Heavy Chains/genetics ; Immunoglobulin Heavy Chains/immunology ; Immunoglobulin Variable Region/genetics ; Immunoglobulin Variable Region/immunology ; Mice ; Mice, Inbred C57BL ; Spleen/immunology
Chemical Substances	Antibodies ; Immunoglobulin Heavy Chains ; Immunoglobulin Variable Region
Language	English
Publishing date	2018-01-29
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.1700568
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Article ; Online: A20 binding and inhibitor of nuclear factor kappa B (NF-κB)-1 (ABIN-1): a novel modulator of mitochondrial autophagy.

Merline, Rosetta / Rödig, Heiko / Zeng-Brouwers, Jinyang / Poluzzi, Chiara / Tascher, Georg / Michaelis, Jonas / Lopez-Mosqueda, Jaime / Rhiner, Andrew / Huber, Lisa Sophie / Diehl, Valentina / Dikic, Ivan / Kögel, Donat / Münch, Christian / Wygrecka, Malgorzata / Schaefer, Liliana

American journal of physiology. Cell physiology

2022 Volume 324, Issue 2, Page(s) C339–C352

Abstract: A20 binding inhibitor of nuclear factor kappa B (NF-κB)-1 (ABIN-1), a polyubiquitin-binding protein ...

Abstract	A20 binding inhibitor of nuclear factor kappa B (NF-κB)-1 (ABIN-1), a polyubiquitin-binding protein, is a signal-induced autophagy receptor that attenuates NF-κB-mediated inflammation and cell death. The present study aimed to elucidate the potential role of ABIN-1 in mitophagy, a biological process whose outcome is decisive in diverse physiological and pathological settings. Microtubule-associated proteins 1A/1B light chain 3B-II (LC3B-II) was found to be in complex with ectopically expressed hemagglutinin (HA)-tagged-full length (FL)-ABIN-1. Bacterial expression of ABIN-1 and LC3A and LC3B showed direct binding of ABIN-1 to LC3 proteins, whereas mutations in the LC3-interacting region (LIR) 1 and 2 motifs of ABIN-1 abrogated ABIN-1/LC3B-II complex formation. Importantly, induction of autophagy in HeLa cells resulted in colocalization of ABIN-1 with LC3B-II in autophagosomes and with lysosomal-associated membrane protein 1 (LAMP-1) in autophagolysosomes, leading to degradation of ABIN-1 with p62. Interestingly, ABIN-1 was found to translocate to damaged mitochondria in HeLa-mCherry-Parkin transfected cells. In line with this observation, clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (Cas9)-mediated deletion of ABIN-1 significantly inhibited the degradation of the mitochondrial outer membrane proteins voltage-dependent anion-selective channel 1 (VDAC-1), mitofusin-2 (MFN2), and translocase of outer mitochondrial membrane (TOM)20. In addition, short interfering RNA (siRNA)-mediated knockdown of ABIN-1 significantly decreased lysosomal uptake of mitochondria in HeLa cells expressing mCherry-Parkin and the fluorescence reporter mt-mKEIMA. Collectively, our results identify ABIN-1 as a novel and selective mitochondrial autophagy regulator that promotes mitophagy, thereby adding a new player to the complex cellular machinery regulating mitochondrial homeostasis.
MeSH term(s)	Humans ; NF-kappa B/metabolism ; HeLa Cells ; Protein Binding ; Mitochondria/metabolism ; Autophagy ; Ubiquitin-Protein Ligases/metabolism
Chemical Substances	NF-kappa B ; Ubiquitin-Protein Ligases (EC 2.3.2.27)
Language	English
Publishing date	2022-11-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	392098-7
ISSN	1522-1563 ; 0363-6143
ISSN (online)	1522-1563
ISSN	0363-6143
DOI	10.1152/ajpcell.00493.2022
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