26 results on '"Tarrab E"'
Search Results
2. 136 Role of mitochondrial permeability transition (MPT) and oxidative stress in cold ischemia/warm reperfusion (CI/WR) injury of rat livers
- Author
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Huet, P.M., primary, Tarrab, E., additional, and Brault, A., additional
- Published
- 2004
- Full Text
- View/download PDF
3. Antigenic diversity of eastern Canadian isolates of infectious pancreatic necrosis virus
- Author
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Tarrab, E, primary, Heppell, J, additional, Berthiaume, L, additional, and Lecomte, J, additional
- Published
- 1996
- Full Text
- View/download PDF
4. Characterization of the small open reading frame on genome segment A of infectious pancreatic necrosis virus
- Author
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Heppell, J., primary, Tarrab, E., additional, Berthiaume, L., additional, Lecomte, J., additional, and Arella, M., additional
- Published
- 1995
- Full Text
- View/download PDF
5. Evidence of a major neutralizable conformational epitope region on VP2 of infectious pancreatic necrosis virus
- Author
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Tarrab, E., primary, Berthiaume, L., additional, Grothe, S., additional, O'Connor-McCourt, M., additional, Heppell, J., additional, and Lecomte, J., additional
- Published
- 1995
- Full Text
- View/download PDF
6. Antigenic characterization of serogroup 'A' of infectious pancreatic necrosis virus with three panels of monoclonal antibodies
- Author
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Tarrab, E., primary, Berthiaume, L., additional, Heppell, J., additional, Arella, M., additional, and Lecomte, J., additional
- Published
- 1993
- Full Text
- View/download PDF
7. Evidence of genomic variations between infectious pancreatic necrosis virus strains determined by restriction fragment profiles
- Author
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Heppell, J., primary, Berthiaume, L., additional, Tarrab, E., additional, Lecomte, J., additional, and Arella, M., additional
- Published
- 1992
- Full Text
- View/download PDF
8. Defining research in mother tongue education
- Author
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Gagné, G., Daems, F., Kroon, S., Sturm, J., Tarrab, E., and Tilburg School of Humanities and Digital Sciences
- Subjects
ComputingMilieux_LEGALASPECTSOFCOMPUTING - Published
- 1987
9. Understanding teaching the mother tongue: Explorations in historical and international comparison
- Author
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Kroon, S., Sturm, J., Gagne, G., Daems, F., Tarrab, E., and Tilburg School of Humanities and Digital Sciences
- Subjects
ComputingMilieux_LEGALASPECTSOFCOMPUTING - Published
- 1987
10. La teoría del preconsciente y la investigación sistemática del discurso en psicoanálisis.
- Author
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Maldavsky, D., Bodni, O., Buceta, C., Cusien, I., Garzoli, E., de Widder, F. Lambersky, Roitman, C. R., de Stanley, C. Tate, Tarrab, E., and de Manson, M. Truscello
- Published
- 2004
11. Cyclophilin D Regulates Antiviral CD8 + T Cell Survival in a Cell-Extrinsic Manner.
- Author
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Condotta SA, Downey J, Pardy RD, Valbon SF, Tarrab E, Lamarre A, Divangahi M, and Richer MJ
- Subjects
- Adoptive Transfer methods, Animals, CD8 Antigens metabolism, Peptidyl-Prolyl Isomerase F genetics, Female, Host Microbial Interactions immunology, Lymphocytic Choriomeningitis therapy, Lymphocytic Choriomeningitis virology, Macrophages immunology, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Mitochondria immunology, Mitochondria metabolism, Receptors, Antigen, T-Cell genetics, Receptors, Antigen, T-Cell metabolism, Signal Transduction genetics, CD8-Positive T-Lymphocytes immunology, Cell Survival genetics, Peptidyl-Prolyl Isomerase F metabolism, Host Microbial Interactions genetics, Lymphocytic Choriomeningitis immunology, Lymphocytic choriomeningitis virus immunology
- Abstract
CD8
+ T cell-mediated immunity is critical for host defense against viruses and requires mitochondria-mediated type I IFN (IFN-I) signaling for optimal protection. Cyclophilin D (CypD) is a mitochondrial matrix protein that modulates the mitochondrial permeability transition pore, but its role in IFN-I signaling and CD8+ T cell responses to viral infection has not been previously explored. In this study, we demonstrate that CypD plays a critical extrinsic role in the survival of Ag-specific CD8+ T cell following acute viral infection with lymphocytic choriomeningitis virus in mice. CypD deficiency resulted in reduced IFN-I and increased CD8+ T cell death, resulting in a reduced antiviral CD8+ T cell response. In addition, CypD deficiency was associated with an increase in pathogen burden at an early time-point following infection. Furthermore, our data demonstrate that transfer of wild-type macrophages (expressing CypD) to CypD-deficient mice can partially restore CD8+ T cell responses. These results establish that CypD plays an extrinsic role in regulating optimal effector CD8+ T cell responses to viral infection. Furthermore, this suggests that, under certain circumstances, inhibition of CypD function may have a detrimental impact on the host's ability to respond to viral infection., (Copyright © 2020 The Authors.)- Published
- 2020
- Full Text
- View/download PDF
12. Efficacy of a Virus-Like Nanoparticle As Treatment for a Chronic Viral Infection Is Hindered by IRAK1 Regulation and Antibody Interference.
- Author
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Chartrand K, Lebel MÈ, Tarrab E, Savard P, Leclerc D, and Lamarre A
- Abstract
Although vaccination has been an effective way of preventing infections ever since the eighteenth century, the generation of therapeutic vaccines and immunotherapies is still a work in progress. A number of challenges impede the development of these therapeutic approaches such as safety issues related to the administration of whole pathogens whether attenuated or inactivated. One safe alternative to classical vaccination methods gaining recognition is the use of nanoparticles, whether synthetic or naturally derived. We have recently demonstrated that the papaya mosaic virus (PapMV)-like nanoparticle can be used as a prophylactic vaccine against various viral and bacterial infections through the induction of protective humoral and cellular immune responses. Moreover, PapMV is also very efficient when used as an immune adjuvant in an immunotherapeutic setting at slowing down the growth of aggressive mouse melanoma tumors in a type I interferon (IFN-I)-dependent manner. In the present study, we were interested in exploiting the capacity of PapMV of inducing robust IFN-I production as treatment for the chronic viral infection model lymphocytic choriomeningitis virus (LCMV) clone 13 (Cl13). Treatment of LCMV Cl13-infected mice with two systemic administrations of PapMV was ineffective, as shown by the lack of changes in viral titers and immune response to LCMV following treatment. Moreover, IFN-α production following PapMV administration was almost completely abolished in LCMV-infected mice. To better isolate the mechanisms at play, we determined the influence of a pretreatment with PapMV on secondary PapMV administration, therefore eliminating potential variables emanating from the infection. Pretreatment with PapMV led to the same outcome as an LCMV infection in that IFN-α production following secondary PapMV immunization was abrogated for up to 50 days while immune activation was also dramatically impaired. We showed that two distinct and overlapping mechanisms were responsible for this outcome. While short-term inhibition was partially the result of interleukin-1 receptor-associated kinase 1 degradation, a crucial component of the toll-like receptor 7 signaling pathway, long-term inhibition was mainly due to interference by PapMV-specific antibodies. Thus, we identified a possible pitfall in the use of virus-like particles for the systemic treatment of chronic viral infections and discuss mitigating alternatives to circumvent these potential problems.
- Published
- 2018
- Full Text
- View/download PDF
13. Complement Component 3 Regulates IFN-α Production by Plasmacytoid Dendritic Cells following TLR7 Activation by a Plant Virus-like Nanoparticle.
- Author
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Lebel MÈ, Langlois MP, Daudelin JF, Tarrab E, Savard P, Leclerc D, and Lamarre A
- Subjects
- Animals, Dendritic Cells metabolism, Enzyme-Linked Immunosorbent Assay, Female, Flow Cytometry, Membrane Glycoproteins metabolism, Mice, Mice, Inbred C57BL, Nanoparticles, Phagocytosis immunology, Polymerase Chain Reaction, Toll-Like Receptor 7 metabolism, Complement C3 immunology, Dendritic Cells immunology, Interferon-gamma biosynthesis, Membrane Glycoproteins immunology, Mosaic Viruses immunology, Toll-Like Receptor 7 immunology
- Abstract
The increasing use of plant viruses for the development of new vaccines and immunotherapy approaches poses questions regarding the mechanism by which the mammalian immune system recognizes these viruses. For example, although natural Abs (NA) and complement are key components of the innate immune system involved in the opsonization, phagocytosis, and destruction of microorganisms infecting mammals, their implication in plant virus recognition and immunogenicity is not well defined. In this study, we address the involvement of NA and the complement system in the activation of innate immunity through engagement of TLR7 with papaya mosaic virus (PapMV)-like nanoparticles. We demonstrate that NA, although binding to PapMV, are not involved in its recognition by the immune system. On the other hand, C3 strongly binds to PapMV nanoparticles and its depletion significantly reduces PapMV's interaction with immune cells. Unexpectedly, however, we observed increased immune cell activation following administration of PapMV to complement-depleted mice. TLR7 activation by PapMV in the absence of C3 induced higher IFN-α production, resulting in superior immune cell activation and increased immunotherapeutic properties. In conclusion, in this study we established the involvement of the complement system in the recognition and the phagocytosis of PapMV nanoparticles and identified an unsuspected role for C3 in regulating the production of IFN-α following TLR7 activation., (Copyright © 2016 by The American Association of Immunologists, Inc.)
- Published
- 2017
- Full Text
- View/download PDF
14. Type I Interferon Impairs Specific Antibody Responses Early during Establishment of LCMV Infection.
- Author
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Daugan M, Murira A, Mindt BC, Germain A, Tarrab E, Lapierre P, Fritz JH, and Lamarre A
- Abstract
Elicitation of type I interferon (IFN-I) has been shown to both enhance and impair cell-mediated immune responses in acute and persistent viral infections, respectively. Here, we show that, in addition to its effect on T cells, IFN-I drives impairment of specific antibody responses through interaction with B cells in the acute phase of lymphocytic choriomeningitis virus (LCMV) infection. This impairment was limited to the T cell-dependent B cell response and was associated with disruption of B cell follicles, development of hypergammaglobulinemia (HGG), and expansion of the T follicular helper cell population. Antigen-specific antibody responses were restored by ablation of IFN-I signaling through antibody-mediated IFN-I receptor blockade and B cell-specific IFN-I receptor knockout. Importantly, IFN-I receptor deficiency in B cells also accelerated the development of LCMV neutralizing antibodies and alleviated HGG. These results provide a potential therapeutic target toward efficient treatment measures that limit immunopathology in persistent viral infections.
- Published
- 2016
- Full Text
- View/download PDF
15. Dok-1 and Dok-2 Regulate the Formation of Memory CD8+ T Cells.
- Author
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Laroche-Lefebvre C, Yousefi M, Daudelin JF, Charpentier T, Tarrab E, Klinck R, Lamarre A, Labrecque N, Stäger S, and Duplay P
- Subjects
- Adaptor Proteins, Signal Transducing genetics, Animals, CD8-Positive T-Lymphocytes virology, Cell Differentiation, Cell Survival, Cells, Cultured, DNA-Binding Proteins genetics, Lymphocyte Activation immunology, Mice, Mice, Inbred C57BL, Mice, Knockout, Phosphoproteins genetics, RNA-Binding Proteins genetics, Receptors, Antigen, T-Cell, alpha-beta metabolism, Signal Transduction, Adaptor Proteins, Signal Transducing metabolism, CD8-Positive T-Lymphocytes immunology, DNA-Binding Proteins metabolism, Immunologic Memory, Phosphoproteins metabolism, RNA-Binding Proteins metabolism, Vaccinia immunology, Virus Diseases immunology
- Abstract
Diverse signals received by CD8
+ T cells are integrated to achieve the required magnitude of cell expansion and the appropriate balance of effector/memory CD8+ T cell generation. Notably, the strength and nature of TCR signaling influence the differentiation and functional capacity of effector and memory CD8+ T cells. Dok-1 and Dok-2, the two members of the Dok family expressed in T cells, negatively regulate TCR signaling in vitro. However, the role of Dok proteins in modulating T cell function in vivo has not yet studied. We studied the function of Dok-1 and Dok-2 proteins in the regulation of the CD8+ T cell response to vaccinia virus infection. Comparison of responses to vaccinia virus expressing OVA peptide SIINFEKL by wild-type and Dok-1/2-/- CD8+ OT-I cells showed that the absence of Dok-1 and Dok-2 slightly reduced the magnitude of virus-specific effector CD8+ T cell expansion. This was not due to reduced proliferation or enhanced apoptosis of effector CD8+ T cells. Dok-1/2-deficient effector CD8+ T cells showed increased cell surface TCR expression following virus infection in vivo and increased expression of granzyme B and TNF upon stimulation with peptide Ag ex vivo. Finally, Dok-1/2-deficient effector CD8+ T had a severe defect in survival that resulted in impaired generation of memory CD8+ T cells. These results reveal the critical involvement of Dok-1 and Dok-2 in a negative-feedback loop that prevents overactivation of CD8+ T cells and promotes memory formation., (Copyright © 2016 by The American Association of Immunologists, Inc.)- Published
- 2016
- Full Text
- View/download PDF
16. Potentiating Cancer Immunotherapy Using Papaya Mosaic Virus-Derived Nanoparticles.
- Author
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Lebel MÈ, Chartrand K, Tarrab E, Savard P, Leclerc D, and Lamarre A
- Subjects
- Animals, CD8-Positive T-Lymphocytes immunology, Cancer Vaccines immunology, Carica virology, Cell Line, Tumor, Cytokines immunology, Female, Immunotherapy, Melanoma immunology, Melanoma pathology, Mice, Inbred C57BL, Mosaic Viruses chemistry, Adjuvants, Immunologic therapeutic use, Cancer Vaccines therapeutic use, Melanoma prevention & control, Mosaic Viruses immunology, Nanoparticles chemistry
- Abstract
The recent development of novel immunotherapies is revolutionizing cancer treatment. These include, for example, immune checkpoint blockade, immunomodulation, or therapeutic vaccination. Although effective on their own, combining multiple approaches will most likely be required in order to achieve the maximal therapeutic benefit. In this regard, the papaya mosaic virus nanoparticle (PapMV) has shown tremendous potential as (i) an immunostimulatory molecule, (ii) an adjuvant, and (iii) a vaccine platform through its intrinsic capacity to activate the innate immune response in an IFN-α-dependent manner. Here, we demonstrate that intratumor administration of PapMV significantly slows down melanoma progression and prolongs survival. This correlates with enhanced chemokine and pro-inflammatory-cytokine production in the tumor and increased immune-cell infiltration. Proportions of total and tumor-specific CD8(+) T cells dramatically increase following PapMV treatment whereas those of myeloid-derived suppressor cells (MDSC) concomitantly decrease. Moreover, systemic PapMV administration prevents metastatic tumor-implantation in the lungs. Importantly, PapMV also synergistically improves the therapeutic benefit of dendritic cell (DC)-based vaccination and PD-1 blockade by potentiating antitumor immune responses. This study illustrates the immunostimulatory potential of a plant virus-derived nanoparticle for cancer therapy either alone or in conjunction with other promising immunotherapies in clinical development.
- Published
- 2016
- Full Text
- View/download PDF
17. Expression of Viral Antigen by the Liver Leads to Chronic Infection Through the Generation of Regulatory T Cells.
- Author
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Lapierre P, Janelle V, Langlois MP, Tarrab E, Charpentier T, and Lamarre A
- Abstract
Background & Aims: The constant exposure of the liver to food and bacterial antigens through the mesenteric circulation requires it to maintain tolerance while preserving the ability to mount an effective immune response against pathogens. We investigated the contribution of the liver's tolerogenic nature on the establishment of chronic viral infections., Methods: TTR-NP mice, which express the nucleoprotein (NP) of lymphocytic choriomeningitis virus (LCMV) specifically in hepatocytes under control of a modified transthyretin (TTR) promoter, were infected with the Armstrong (Arm) or WE acute strains of LCMV., Results: The infection persisted for at least 147 days in TTR-NP mice. Expression of NP by the liver induced a strong peripheral tolerance against NP that was mediated by interleukin-10-secreting CD4
+ regulatory T cells, leading to high PD-1 (programmed death-1) expression and reduced effector function of virus-specific T cells. Despite an active immune response against LCMV, peripheral tolerance against a single viral protein was sufficient to induce T-cell exhaustion and chronic LCMV Armstrong (Arm) or WE infection by limiting the antiviral T-cell response in an otherwise immunocompetent host. Regulatory T-cell depletion of chronically infected TTR-NP mice led to functional restoration of LCMV-specific CD4+ and CD8+ T cell responses and viral clearance., Conclusions: Expression of a viral antigen by hepatocytes can induce a state of peripheral tolerance mediated by regulatory T cells that can lead to the establishment of a chronic viral infection. Strategies targeting regulatory T cells in patients chronically infected with hepatotropic viruses could represent a promising approach to restore functional antiviral immunity and clear infection.- Published
- 2015
- Full Text
- View/download PDF
18. Transient complement inhibition promotes a tumor-specific immune response through the implication of natural killer cells.
- Author
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Janelle V, Langlois MP, Tarrab E, Lapierre P, Poliquin L, and Lamarre A
- Subjects
- Animals, CD8-Positive T-Lymphocytes immunology, Cell Line, Tumor, Killer Cells, Natural immunology, Mice, Mice, Inbred C57BL, Signal Transduction drug effects, Spleen immunology, Complement C3 immunology, Complement Inactivating Agents pharmacology, Elapid Venoms pharmacology, Melanoma, Experimental drug therapy, Melanoma, Experimental immunology
- Abstract
Although the role of the complement system in cancer development has been studied, its involvement in the development of an antitumoral immune response remains poorly understood. Using cobra venom factor (CVF) to inhibit the complement cascade via C3 molecule exhaustion in immunocompetent mice bearing B16gp33 melanoma tumors, we show that transient inhibition of the complement system allowed for the development of a more robust gp33-specific antitumoral CD8(+) T-cell response. This immune response proved to be natural killer (NK) dependent, suggesting an interaction of complement proteins with this cellular subset leading to T lymphocyte activation and enhanced cytotoxic T-cell activity against tumor cells. This study demonstrates for the first time the implication of the complement system in the development of NK-mediated cytotoxic T-cell-dependent antitumoral immune responses. The complement pathway could therefore be a potent therapeutic target to improve NK-dependent antitumoral immune responses in patients with cancer., (©2013 AACR.)
- Published
- 2014
- Full Text
- View/download PDF
19. Nanoparticle adjuvant sensing by TLR7 enhances CD8+ T cell-mediated protection from Listeria monocytogenes infection.
- Author
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Lebel MÈ, Daudelin JF, Chartrand K, Tarrab E, Kalinke U, Savard P, Labrecque N, Leclerc D, and Lamarre A
- Subjects
- Adaptive Immunity, Animals, Dendritic Cells immunology, Drug Evaluation, Preclinical, Female, Immunoglobulin G biosynthesis, Immunologic Memory, Interferon Type I immunology, Listeriosis immunology, Membrane Glycoproteins deficiency, Membrane Glycoproteins immunology, Mice, Mice, Inbred C57BL, Myeloid Differentiation Factor 88 deficiency, Myeloid Differentiation Factor 88 immunology, Nanoparticles, Ovalbumin immunology, RNA, Viral immunology, Receptor, Interferon alpha-beta deficiency, Toll-Like Receptor 7 deficiency, Toll-Like Receptor 7 immunology, Tymovirus genetics, Adjuvants, Immunologic, CD8-Positive T-Lymphocytes immunology, Listeria monocytogenes immunology, Listeriosis prevention & control, Membrane Glycoproteins agonists, T-Lymphocyte Subsets immunology, Toll-Like Receptor 7 agonists, Tymovirus immunology, Vaccination
- Abstract
Developing new adjuvants and vaccination strategies is of paramount importance to successfully fight against many life-threatening infectious diseases and cancer. Very few adjuvants are currently authorized for human use, and these mainly stimulate a humoral response. However, specific Abs are not sufficient to confer protection against persisting infections or cancer. Therefore, development of adjuvants and immunomodulators able to enhance cell-mediated immune responses represents a major medical need. We recently showed that papaya mosaic virus nanoparticles (PapMV), self-assembled from the coat protein of a plant virus and a noncoding ssRNA molecule, are highly immunogenic in mice. PapMV can be used either as a vaccine delivery platform, through fusion of various epitopes to the coat protein or as adjuvant to enhance humoral immune responses against coadministered Ags or vaccines. However, the mechanisms that confer these immunomodulatory properties to PapMV and its ability to enhance T cell vaccines remain unknown. Using immunization studies in mice, we demonstrate in this paper that PapMV represents a novel TLR7 agonist with strong immunostimulatory properties. More importantly, pretreatment with PapMV significantly improves effector and memory CD8(+) T cell responses generated through dendritic cell vaccination increasing protection against a Listeria monocytogenes challenge.
- Published
- 2014
- Full Text
- View/download PDF
20. Cyclosporin-A does not prevent cold ischemia/reperfusion injury of rat livers.
- Author
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Tarrab E, Huet PM, Brault A, Rocheleau B, Laurens M, and Crenesse D
- Subjects
- Adenosine pharmacology, Allopurinol pharmacology, Animals, Apoptosis drug effects, Caspase 3 metabolism, Cyclosporine pharmacology, Dimethyl Sulfoxide pharmacology, Endothelium drug effects, Endothelium pathology, Glutathione pharmacology, Hepatocytes drug effects, Hepatocytes pathology, Insulin pharmacology, Liver enzymology, Liver Transplantation pathology, Male, Models, Animal, Organ Preservation Solutions pharmacology, Raffinose pharmacology, Rats, Rats, Inbred Lew, Regional Blood Flow physiology, Reperfusion Injury enzymology, Cold Ischemia, Cyclosporine therapeutic use, Liver blood supply, Liver pathology, Reperfusion Injury pathology, Reperfusion Injury prevention & control
- Abstract
Cyclosporin-A (CsA) has been reported to protect livers from warm ischemia/reperfusion (I/R) injury. To study if CsA has also a protective effect on cold I/R injury, two models were used: the isolated perfused rat liver (IPRL) and the orthotopic rat liver transplantation (ORLT). (1) IPRL: Livers were preserved for 24 h (5°C) in University of Wisconsin (UW) solution alone (group 1), with CsA (400 nM) dissolved in dimethylsulfoxide (50 μM) (group 2), and with dimethylsulfoxide (DMSO) alone (group 3). Livers were reperfused for 60 min (37°C) (n = 8/group). Cell necrosis was evaluated by trypan blue uptake and apoptosis by laddering and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay, and by caspase-3 activation. Marked and similar sinusoidal endothelial cell necrosis was found in the three groups while apoptosis was found similarly deceased in groups 2 and 3 compared with group 1. (2) ORLT: Donors received either CsA (5 mg/kg) or corn oil 24 h before transplantation. Recipients were sacrificed after 240 min; cell necrosis and apoptosis were then evaluated. No difference was found between treated and control groups. The current data strongly suggest that CsA has no protective effect on hepatic cold I/R injury. Hepatocyte apoptosis can be reduced by antioxidants, as occurred with DMSO, but introduction of CsA does not provide additional protective effect., (Copyright © 2012 Elsevier Inc. All rights reserved.)
- Published
- 2012
- Full Text
- View/download PDF
21. The outcome of cross-priming during virus infection is not directly linked to the ability of the antigen to be cross-presented.
- Author
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Alatery A, Tarrab E, Lamarre A, and Basta S
- Subjects
- Animals, Antigens, Viral immunology, Antigens, Viral metabolism, Cell Line, Cell Proliferation, Dendritic Cells immunology, Dendritic Cells virology, Humans, Immunodominant Epitopes immunology, Immunodominant Epitopes metabolism, Lymphocyte Activation, Lymphocytic choriomeningitis virus pathogenicity, Macrophages immunology, Macrophages virology, Mice, Mice, Inbred C57BL, Peptide Fragments immunology, Peptide Fragments metabolism, T-Lymphocytes, Cytotoxic immunology, T-Lymphocytes, Cytotoxic pathology, Arenaviridae Infections immunology, Cross-Priming, Dendritic Cells metabolism, Lymphocytic choriomeningitis virus immunology, Macrophages metabolism, T-Lymphocytes, Cytotoxic metabolism
- Abstract
The initiation of CD8(+) T cell (CTL) immune responses can occur via cross-priming. Recent data suggested a relationship between cross-presentation and immunodominance of epitope-specific T cells. To test this association, we evaluated the efficacy of cross-presentation for several virus epitopes in vitro and examined if this can be extrapolated in vivo. Employing lymphocytic choriomeningitis virus (LCMV), we demonstrate that the cross-presentation and cross-priming of LCMV antigens were dominated by NP396, but not NP205 when analyzing the LCMV-NP. Although with LCMV-GP, cross-presentation was dominated by GP276, and cross-priming was dominated by GP33. Importantly, although NP396 was significantly more efficient than GP33 in cross-presentation, cross-priming of their specific CTL was comparable. In a subsequent virus challenge after cross-priming, GP33-specific CTL dominated the response. Accordingly, based on our data, the ability of viral epitopes to be cross-presented in vitro does not entirely reflect what would occur in cross-priming. Thus, weak cross-presenting antigens may still cross-prime an efficient CTL response depending on other in vivo elements such as the naïve T-cell precursor frequencies.
- Published
- 2010
- Full Text
- View/download PDF
22. Altered immunodominance hierarchies of CD8+ T cells in the spleen after infection at different sites is contingent on high virus inoculum.
- Author
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Siddiqui S, Tarrab E, Lamarre A, and Basta S
- Subjects
- Animals, Cytokines biosynthesis, Mice, Mice, Inbred C57BL, Arenaviridae Infections immunology, CD8-Positive T-Lymphocytes immunology, Lymphocytic choriomeningitis virus immunology, Spleen immunology
- Abstract
Activated epitope-specific CD8+ T cells after virus infection can be organized into hierarchies (immunodominance), based on their ability to focus the response on few viral determinants. The mechanisms responsible for immunodominance can be multifactorial, with CD8+ T cells precursor frequencies recently highlighted as a key regulator. Employing the LCMV infection model, we demonstrate that the hierarchies were altered when comparing different sites of infection but only at high viral doses. These findings have significant implications when investigating immunity to viruses with different replication abilities that may override the influence of T cell precursor frequencies., (Copyright 2010 Elsevier Masson SAS. All rights reserved.)
- Published
- 2010
- Full Text
- View/download PDF
23. Sinusoidal endothelial cell and hepatocyte death following cold ischemia-warm reperfusion of the rat liver.
- Author
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Huet PM, Nagaoka MR, Desbiens G, Tarrab E, Brault A, Bralet MP, and Bilodeau M
- Subjects
- Animals, Caspase 3, Caspases metabolism, Cell Survival, Cold Temperature, Endothelium metabolism, Hepatocytes metabolism, Hot Temperature, Indicator Dilution Techniques, Liver blood supply, Liver pathology, Liver Transplantation, Male, Microcirculation, Necrosis, Rats, Rats, Inbred Lew, Apoptosis, Cryopreservation, Endothelium pathology, Hepatocytes pathology, Reperfusion Injury pathology
- Abstract
Cold ischemia-warm reperfusion (CI-WR) injury of the liver is characterized by marked alterations of sinusoidal endothelial cells (SECs), whereas hepatocytes appear to be relatively unscathed. However, the time course and mechanism of cell death remain controversial: early versus late phenomenon, necrosis versus apoptosis? We describe the occurrence and nature of cell death after different periods of CI with University of Wisconsin (UW) solution and after different periods of WR in the isolated perfused rat liver model. After 24- and 42-hour CI (viable and nonviable livers, respectively), similar patterns of liver cell death were seen: SEC necrosis appeared early after WR (10 minutes) and remained stable for up to 120 minutes. After 30 minutes of WR, apoptosis increased progressively with WR length. Based on morphological criteria, apoptotic cells were mainly hepatocytes within liver plates or extruded in the sinusoidal lumen. In addition, only after 42-hour CI were large clusters of necrotic hepatocytes found in areas of congested sinusoids. In these same livers, the hepatic microcirculation, evaluated by means of the multiple-indicator dilution technique, revealed extracellular matrix disappearance with no-flow areas. In conclusion, different time courses and mechanisms of cell death occur in rat livers after CI-WR, with early SEC necrosis followed by delayed hepatocyte apoptosis. These processes do not appear to be of major importance in the mechanism of graft failure because they are similar under both nonlethal and lethal conditions; this is not the case for the loss of the extracellular matrix found only under lethal conditions and associated with hepatocyte necrosis.
- Published
- 2004
- Full Text
- View/download PDF
24. Strain variability and localization of important epitopes on the major structural protein (VP2) of infectious pancreatic necrosis virus.
- Author
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Heppell J, Tarrab E, Lecomte J, Berthiaume L, and Arella M
- Subjects
- Amino Acid Sequence, Animals, Antibodies, Monoclonal immunology, Base Sequence, Capsid analysis, Capsid immunology, Capsid Proteins, DNA Primers, Epitopes analysis, Epitopes immunology, Infectious pancreatic necrosis virus genetics, Molecular Sequence Data, Mutation, Sequence Homology, Amino Acid, Species Specificity, Capsid genetics, Epitopes genetics, Genetic Variation, Infectious pancreatic necrosis virus immunology
- Abstract
Infectious pancreatic necrosis virus (IPNV), a birnavirus, is an important pathogen in fish farms. Analyses of viral proteins showed that VP2 is the major structural and immunogenic polypeptide of the virus. All neutralizing monoclonal antibodies (mAbs) against IPNV are specific to VP2 and bind to continuous or discontinuous epitopes. In order to determine which parts of the protein are involved in antigenic variations, five IPNV strains were sequenced over the VP2 coding region. Comparison of the sequences obtained with three previously published strains revealed a central variable domain (positions 183 to 335) which encompasses two hydrophilic hypervariable segments. Viral mutants which escaped neutralization were then selected with anti-VP2 mAbs directed against discontinuous epitopes. Sequencing of three mutants revealed a single amino acid mismatch in each of them. All of these substitutions occurred in the hypervariable segments, suggesting that these regions are involved in the formation of a discontinuous epitope. Finally, expression of different truncated VP2s in Escherichia coli allowed localization of the binding site for neutralizing mAbs which recognize continuous epitopes. One of these mAbs bound to the region adjacent to the C-terminus of the variable domain of VP2, while two others reacted with the central and C-terminal parts of the variable domain. No antibody reacted with the N-terminus of VP2. These results suggest that the variable domain of VP2 and the 20 adjacent amino acids of the conserved C-terminal part are the most important in inducing an immune response for the protection of animals.
- Published
- 1995
- Full Text
- View/download PDF
25. Comparison of amino acid sequences deduced from a cDNA fragment obtained from infectious pancreatic necrosis virus (IPNV) strains of different serotypes.
- Author
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Heppell J, Berthiaume L, Corbin F, Tarrab E, Lecomte J, and Arella M
- Subjects
- Amino Acid Sequence, Animals, Cell Line, Genome, Viral, Molecular Sequence Data, Polymerase Chain Reaction, RNA Viruses genetics, Sequence Homology, Amino Acid, Serotyping, Species Specificity, Genetic Variation, RNA Viruses classification
- Abstract
Infectious pancreatic necrosis is an important viral disease of salmonid fish reared in hatchery. Its etiological agent, IPNV, showed a high degree of antigenic heterogeneity. Up to 10 serotypes and 2 serogroups were proposed. Yet, very little is known about genomic variations among viruses of different origin. In order to investigate these variations, a 310-bp cDNA fragment was prepared from 17 IPNV strains by reverse transcription of the viral genome and amplification by the polymerase chain reaction. These fragments were then cloned and sequenced. Comparison of the 17 sequences obtained with 3 previously published ones, at the amino acid level, showed that serologically related viruses are highly homologous (over 96% homology) but some strains which were reported to belong to different serotypes also appeared closely related. Thus, only three major groups, clearly distinct from each other, could be formed. Apart from this, a search for the exact cleavage site of the unprocessed polyprotein of IPNV was done since the amplified fragment used for sequencing was localized at the junction between two polypeptides of the virus, pVP2 and NS. No obvious sequence or dipeptide appeared conserved in all birnaviruses.
- Published
- 1993
- Full Text
- View/download PDF
26. Antigenic and genomic differences of two Jasper strains of infectious pancreatic necrosis virus.
- Author
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Berthiaume L, Tarrab E, Heppell J, Arella M, Dobos P, Duncan R, and Lecomte J
- Subjects
- Animals, Cells, Cultured, DNA, Viral genetics, DNA, Viral metabolism, Deoxyribonucleases, Type II Site-Specific metabolism, Enzyme-Linked Immunosorbent Assay, Fishes, Neutralization Tests, Reoviridae genetics, Reoviridae immunology, Sequence Homology, Nucleic Acid, Antigens, Viral, Genome, Viral, Reoviridae classification
- Abstract
Strains of infectious pancreatic necrosis virus (IPNV-Jasper) obtained from two different laboratories were compared serologically with polyclonal and monoclonal antibodies. Nucleotide sequence and restriction endonuclease patterns of 359-bp fragment of genome segment A cDNA were also compared. Substantial differences were found in both analyses that will support the fact that the two Jasper strains are not identical.
- Published
- 1992
- Full Text
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