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Article ; Online: Distinct intracellular trafficking of hepatitis C virus in myeloid and plasmacytoid dendritic cells.

Lambotin, Mélanie / Baumert, Thomas F / Barth, Heidi

2010 Volume 84, Issue 17, Page(s) 8964–8969

Abstract: Dendritic cells (DCs) are of pivotal importance for the initiation of immune responses to control and eliminate viral infections. The molecular mechanisms of hepatitis C virus (HCV) antigen uptake and processing by blood DCs are poorly defined. Here we ... ...

Abstract	Dendritic cells (DCs) are of pivotal importance for the initiation of immune responses to control and eliminate viral infections. The molecular mechanisms of hepatitis C virus (HCV) antigen uptake and processing by blood DCs are poorly defined. Here we show that human blood DC subsets acquire HCV independent of the classical HCV entry factors. Following HCV uptake, human plasmacytoid and myeloid DC subsets deliver HCV antigen into distinct endocytotic compartments, which are dedicated to presentation to CD4(+) or CD8(+) T cells. Our findings support a model of HCV antigen processing and presentation in which DC subsets fulfill distinct functions.
MeSH term(s)	Cells, Cultured ; Dendritic Cells/immunology ; Dendritic Cells/metabolism ; Dendritic Cells/virology ; Hepacivirus/immunology ; Hepacivirus/physiology ; Hepatitis C/immunology ; Hepatitis C/metabolism ; Hepatitis C/virology ; Hepatitis C Antigens/immunology ; Hepatitis C Antigens/metabolism ; Humans ; Myeloid Cells/immunology ; Myeloid Cells/metabolism ; Myeloid Cells/virology ; Protein Transport
Chemical Substances	Hepatitis C Antigens
Language	English
Publishing date	2010-06-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80174-4
ISSN	1098-5514 ; 0022-538X
ISSN (online)	1098-5514
ISSN	0022-538X
DOI	10.1128/JVI.00517-10
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Article ; Online: A cinnamon-derived procyanidin type A compound inhibits hepatitis C virus cell entry.

Fauvelle, Catherine / Lambotin, Melanie / Heydmann, Laura / Prakash, Ekambaranellore / Bhaskaran, Sunil / Vishwaraman, Mohan / Baumert, Thomas F / Moog, Christiane

Hepatology international

2017 Volume 11, Issue 5, Page(s) 440–445

Abstract: Background and aims: Chronic hepatitis C virus (HCV) infection is a major cause of liver disease worldwide. Although direct-acting antivirals can cure the large majority of treated patients, important limitations remain, including treatment failure and ... ...

Abstract	Background and aims: Chronic hepatitis C virus (HCV) infection is a major cause of liver disease worldwide. Although direct-acting antivirals can cure the large majority of treated patients, important limitations remain, including treatment failure and high costs precluding access to therapy in resource-limited settings. We report herein the anti-HCV effects of IND02, a procyanidin type A molecule, isolated and characterized from cinnamon. Methods and results: Using cellculture-derived HCV (HCVcc), HCV pseudoparticles (HCVpp), and subgenomic replicons, we demonstrated that IND02 markedly and dose-dependently inhibited HCV cell entry. Kinetic assays demonstrated that IND02 inhibits HCV entry most likely at a postbinding step. Experiments performed using primary human hepatocytes confirmed inhibition of HCV entry by IND02, demonstrating the functional impact in the most physiological cell-based system for studying HCV-host interactions. Conclusions: The natural compound IND02 exhibits potent HCV cell entry inhibition and provides a novel perspective for development of a low-cost antiviral for treatment of HCV infection.
MeSH term(s)	Antiviral Agents/pharmacology ; Antiviral Agents/therapeutic use ; Biflavonoids/pharmacology ; Biflavonoids/therapeutic use ; Catechin/pharmacology ; Catechin/therapeutic use ; Cinnamomum zeylanicum ; Dose-Response Relationship, Drug ; Hepacivirus/drug effects ; Hepacivirus/physiology ; Hepatitis C, Chronic/drug therapy ; Humans ; Proanthocyanidins/pharmacology ; Proanthocyanidins/therapeutic use
Chemical Substances	Antiviral Agents ; Biflavonoids ; Proanthocyanidins ; procyanidin (4852-22-6) ; Catechin (8R1V1STN48)
Language	English
Publishing date	2017-07-11
Publishing country	United States
Document type	Journal Article
ZDB-ID	2270316-0
ISSN	1936-0541 ; 1936-0533
ISSN (online)	1936-0541
ISSN	1936-0533
DOI	10.1007/s12072-017-9809-y
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Article ; Online: Antiviral and Immunoregulatory Effects of Indoleamine-2,3-Dioxygenase in Hepatitis C Virus Infection.

Lepiller, Quentin / Soulier, Eric / Li, Qisheng / Lambotin, Mélanie / Barths, Jochen / Fuchs, Dietmar / Stoll-Keller, Françoise / Liang, T Jake / Barth, Heidi

Journal of innate immunity

2015 Volume 7, Issue 5, Page(s) 530–544

Abstract: In patients with hepatitis C virus (HCV) infection, enhanced activity of indoleamine-2,3-dioxygenase 1 (IDO) has been reported. IDO - a tryptophan-catabolizing enzyme - has been considered as both an innate defence mechanism and an important regulator of ...

Abstract	In patients with hepatitis C virus (HCV) infection, enhanced activity of indoleamine-2,3-dioxygenase 1 (IDO) has been reported. IDO - a tryptophan-catabolizing enzyme - has been considered as both an innate defence mechanism and an important regulator of the immune response. The molecular mechanism of IDO induction in HCV infection and its role in the antiviral immune response remain unknown. Using primary human hepatocytes, we show that HCV infection stimulates IDO expression. IDO gene induction was transient and coincided with the expression of types I and III interferons (IFNs) and IFN-stimulated genes in HCV-infected hepatocytes. Overexpression of hepatic IDO prior to HCV infection markedly impaired HCV replication in hepatocytes, suggesting that IDO limits the spread of HCV within the liver. siRNA-mediated IDO knock-down revealed that IDO functions as an IFN-mediated anti-HCV effector. Hepatic IDO was most potently induced by IFN-x03B3;, and ongoing HCV replication could significantly upregulate IDO expression. IRF1 (IFN-regulatory factor 1) and STAT1 (signal transducer and activator of transcription 1) regulated hepatic IDO expression. Hepatic IDO expression also had a significant inhibitory effect on CD4+ T-cell proliferation. Our data suggest that hepatic IDO plays a dual role during HCV infection by slowing down viral replication and also regulating host immune responses.
MeSH term(s)	CD4-Positive T-Lymphocytes/immunology ; Cell Proliferation/genetics ; Cells, Cultured ; Hepacivirus/physiology ; Hepatitis C/immunology ; Hepatocytes/immunology ; Hepatocytes/virology ; Humans ; Immunity, Innate ; Immunosuppression ; Indoleamine-Pyrrole 2,3,-Dioxygenase/metabolism ; Interferon Regulatory Factor-1/genetics ; Interferon Regulatory Factor-1/metabolism ; Interferons/genetics ; Interferons/metabolism ; RNA, Small Interfering/genetics ; STAT1 Transcription Factor/genetics ; STAT1 Transcription Factor/metabolism ; Virus Replication/genetics
Chemical Substances	IDO1 protein, human ; IRF1 protein, human ; Indoleamine-Pyrrole 2,3,-Dioxygenase ; Interferon Regulatory Factor-1 ; RNA, Small Interfering ; STAT1 Transcription Factor ; Interferons (9008-11-1)
Language	English
Publishing date	2015-03-19
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2454158-8
ISSN	1662-8128 ; 1662-811X
ISSN (online)	1662-8128
ISSN	1662-811X
DOI	10.1159/000375161
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Article ; Online: A look behind closed doors: interaction of persistent viruses with dendritic cells.

Lambotin, Mélanie / Raghuraman, Sukanya / Stoll-Keller, Françoise / Baumert, Thomas F / Barth, Heidi

Nature reviews. Microbiology

2010 Volume 8, Issue 5, Page(s) 350–360

Abstract: Persistent infections with HIV, hepatitis B virus and hepatitis C virus are major causes of morbidity and mortality worldwide. As sentinels of the immune system, dendritic cells (DCs) are crucial for the generation of protective antiviral immunity. ... ...

Abstract	Persistent infections with HIV, hepatitis B virus and hepatitis C virus are major causes of morbidity and mortality worldwide. As sentinels of the immune system, dendritic cells (DCs) are crucial for the generation of protective antiviral immunity. Recent advances in our understanding of the role of DCs during infection with these viruses provide insights into the mechanisms used by these viruses to exploit DC function and evade innate and adaptive immunity. In this Review we highlight the current knowledge about the interaction between DCs and these viruses and the underlying mechanisms that might influence the outcome of viral infections.
MeSH term(s)	Antigen Presentation ; Dendritic Cells/classification ; Dendritic Cells/immunology ; Dendritic Cells/virology ; HIV/immunology ; HIV/pathogenicity ; HIV Infections/immunology ; HIV Infections/virology ; Hepacivirus/immunology ; Hepacivirus/pathogenicity ; Hepatitis B/immunology ; Hepatitis B/virology ; Hepatitis B virus/immunology ; Hepatitis B virus/pathogenicity ; Hepatitis C/immunology ; Hepatitis C/virology ; Host-Pathogen Interactions/immunology ; Humans ; Immune Tolerance ; Liver/immunology ; Liver/virology ; Models, Immunological
Language	English
Publishing date	2010-04-07
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2139054-X
ISSN	1740-1534 ; 1740-1526
ISSN (online)	1740-1534
ISSN	1740-1526
DOI	10.1038/nrmicro2332
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Zs.A 5865: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Challenges for HCV vaccine development in HIV-HCV coinfection.

Lambotin, Mélanie / Barth, Heidi / Moog, Christiane / Habersetzer, François / Baumert, Thomas F / Stoll-Keller, Françoise / Fafi-Kremer, Samira

Expert review of vaccines

2012 Volume 11, Issue 7, Page(s) 791–804

Abstract: It is estimated that 4-5 million HIV-infected patients are coinfected with HCV. The impact of HIV on the natural course of HCV infection is deleterious. This includes a higher rate of HCV persistence and a faster rate of fibrosis progression. Coinfected ... ...

Abstract	It is estimated that 4-5 million HIV-infected patients are coinfected with HCV. The impact of HIV on the natural course of HCV infection is deleterious. This includes a higher rate of HCV persistence and a faster rate of fibrosis progression. Coinfected patients show poor treatment outcome following standard HCV therapy. Although direct antiviral agents offer new therapeutic options, their use is hindered by potential drug interactions and toxicity in HIV-infected patients under HAART. Overtime, a large reservoir of HCV genotype 1 patients will accumulate in resource poor countries where the hepatitis C treatment is not easily affordable and HIV therapy remains the primary health issue for coinfected individuals. HCV vaccines represent a promising strategy as an adjunct or alternative to current HCV therapy. Here, the authors review the pathogenesis of hepatitis C in HIV-infected patients, with a focus on the impact of HIV on HCV-specific immune responses and discuss the challenges for vaccine development in HIV-HCV coinfection.
MeSH term(s)	Animals ; Coinfection ; HIV Infections/epidemiology ; Hepacivirus/immunology ; Hepacivirus/pathogenicity ; Hepatitis C/epidemiology ; Hepatitis C/immunology ; Hepatitis C/therapy ; Humans ; Treatment Outcome ; Vaccination ; Viral Hepatitis Vaccines/immunology
Chemical Substances	Viral Hepatitis Vaccines
Language	English
Publishing date	2012-07
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2181284-6
ISSN	1744-8395 ; 1476-0584
ISSN (online)	1744-8395
ISSN	1476-0584
DOI	10.1586/erv.12.52
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Zs.A 6077: Show issues

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Article: Antiviral and Immunoregulatory Effects of Indoleamine-2,3-Dioxygenase in Hepatitis C Virus Infection

Lepiller, Quentin / Soulier, Eric / Li, Qisheng / Lambotin, Mélanie / Barths, Jochen / Fuchs, Dietmar / Stoll-Keller, Françoise / Liang, T. Jake / Barth, Heidi

Journal of Innate Immunity

2015 Volume 7, Issue 5, Page(s) 530–544

Institution	Laboratoire de Virologie, Hôpitaux Universitaires de Strasbourg INSERM U1109 INSERM U1110, and Fédération de Médecine Translationnelle de Strasbourg, Université de Strasbourg, Strasbourg, France Division of Biological Chemistry, Biocentre, Innsbruck Medical University, Innsbruck, Austria Liver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, Md., USA
Abstract	In patients with hepatitis C virus (HCV) infection, enhanced activity of indoleamine-2,3-dioxygenase 1 (IDO) has been reported. IDO - a tryptophan-catabolizing enzyme - has been considered as both an innate defence mechanism and an important regulator of the immune response. The molecular mechanism of IDO induction in HCV infection and its role in the antiviral immune response remain unknown. Using primary human hepatocytes, we show that HCV infection stimulates IDO expression. IDO gene induction was transient and coincided with the expression of types I and III interferons (IFNs) and IFN-stimulated genes in HCV-infected hepatocytes. Overexpression of hepatic IDO prior to HCV infection markedly impaired HCV replication in hepatocytes, suggesting that IDO limits the spread of HCV within the liver. siRNA-mediated IDO knock-down revealed that IDO functions as an IFN-mediated anti-HCV effector. Hepatic IDO was most potently induced by IFN-γ, and ongoing HCV replication could significantly upregulate IDO expression. IRF1 (IFN-regulatory factor 1) and STAT1 (signal transducer and activator of transcription 1) regulated hepatic IDO expression. Hepatic IDO expression also had a significant inhibitory effect on CD4+ T-cell proliferation. Our data suggest that hepatic IDO plays a dual role during HCV infection by slowing down viral replication and also regulating host immune responses.
Keywords	Indoleamine-2,3-dioxygenase ; Hepatocyte ; Hepatitis C virus ; Antiviral immune response
Language	English
Publishing date	2015-03-19
Publisher	S. Karger AG
Publishing place	Basel, Switzerland
Document type	Article
Note	Research Article
ZDB-ID	2454158-8
ISSN	1662-8128 ; 1662-811X
ISSN (online)	1662-8128
ISSN	1662-811X
DOI	10.1159/000375161
Database	Karger publisher's database

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Article ; Online: Dendritic cell-lymphocyte cross talk downregulates host restriction factor SAMHD1 and stimulates HIV-1 replication in dendritic cells.

Su, Bin / Biedma, Marina Elizabeth / Lederle, Alexandre / Peressin, Maryse / Lambotin, Mélanie / Proust, Alizé / Decoville, Thomas / Schmidt, Sylvie / Laumond, Géraldine / Moog, Christiane

Journal of virology

2014 Volume 88, Issue 9, Page(s) 5109–5121

Abstract: Unlabelled: Human immunodeficiency virus type 1 (HIV-1) replication in dendritic cells (DCs) is restricted by SAMHD1. This factor is counteracted by the viral protein Vpx; Vpx is found in HIV-2 and simian immunodeficiency virus (SIV) from sooty ... ...

Abstract	Unlabelled: Human immunodeficiency virus type 1 (HIV-1) replication in dendritic cells (DCs) is restricted by SAMHD1. This factor is counteracted by the viral protein Vpx; Vpx is found in HIV-2 and simian immunodeficiency virus (SIV) from sooty mangabeys (SIVsm) or from macaques (SIVmac) but is absent from HIV-1. We previously observed that HIV-1 replication in immature DCs is stimulated by cocultivation with primary T and B lymphocytes, suggesting that HIV-1 restriction in DCs may be overcome under coculture conditions. Here, we aimed to decipher the mechanism of SAMHD1-mediated restriction in DC-lymphocyte coculture. We found that coculture with lymphocytes downregulated SAMHD1 expression and was associated with increased HIV-1 replication in DCs. Moreover, in infected DC-T lymphocyte cocultures, DCs acquired maturation status and secreted type 1 interferon (alpha interferon [IFN-α]). The blockade of DC-lymphocyte cross talk by anti-ICAM-1 antibody markedly inhibited the stimulation of HIV-1 replication and prevented the downregulation of SAMHD1 expression in cocultured DCs. These results demonstrate that, in contrast to purified DCs, cross talk with lymphocytes downregulates SAMHD1 expression in DCs, triggering HIV-1 replication and an antiviral immune response. Therefore, HIV-1 replication and immune sensing by DCs should be investigated in more physiologically relevant models of DC/lymphocyte coculture. Importance: SAMHD1 restricts HIV-1 replication in dendritic cells (DCs). Here, we demonstrate that, in a coculture model of DCs and lymphocytes mimicking early mucosal HIV-1 infection, stimulation of HIV-1 replication in DCs is associated with downregulation of SAMHD1 expression and activation of innate immune sensing by DCs. We propose that DC-lymphocyte cross talk occurring in vivo modulates host restriction factor SAMHD1, promoting HIV-1 replication in cellular reservoirs and stimulating immune sensing.
MeSH term(s)	Coculture Techniques ; Dendritic Cells/immunology ; Dendritic Cells/virology ; Down-Regulation ; HIV-1/physiology ; Humans ; Lymphocytes/immunology ; Monomeric GTP-Binding Proteins/biosynthesis ; SAM Domain and HD Domain-Containing Protein 1 ; Virus Cultivation ; Virus Replication
Chemical Substances	SAM Domain and HD Domain-Containing Protein 1 (EC 3.1.5.-) ; SAMHD1 protein, human (EC 3.1.5.-) ; Monomeric GTP-Binding Proteins (EC 3.6.5.2)
Language	English
Publishing date	2014-02-26
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80174-4
ISSN	1098-5514 ; 0022-538X
ISSN (online)	1098-5514
ISSN	0022-538X
DOI	10.1128/JVI.03057-13
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Zs.A 609: Show issues

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Article ; Online: Efficient transfer of HIV-1 in trans and in cis from Langerhans dendritic cells and macrophages to autologous T lymphocytes.

Peressin, Maryse / Proust, Alizé / Schmidt, Sylvie / Su, Bin / Lambotin, Mélanie / Biedma, Marina E / Laumond, Géraldine / Decoville, Thomas / Holl, Vincent / Moog, Christiane

AIDS (London, England)

2014 Volume 28, Issue 5, Page(s) 667–677

Abstract: Objective: The chronology of HIV infection in mucosal tissue after sexual transmission is unknown. Several potential HIV target cells are present at these sites, including dendritic cells, macrophages, and CD4(+) T lymphocytes. Dendritic cells and ... ...

Abstract	Objective: The chronology of HIV infection in mucosal tissue after sexual transmission is unknown. Several potential HIV target cells are present at these sites, including dendritic cells, macrophages, and CD4(+) T lymphocytes. Dendritic cells and macrophages are antigen-presenting cells (APCs) and are thus involved in cross-talk with T cells. This close contact may favor efficient HIV-1 transfer to T lymphocytes, resulting in rapid HIV-1 dissemination. Design: We investigated the role of APCs in HIV transfer to T cells by incubating Langerhans cells and interstitial dendritic cells (IDCs) or monocyte-derived macrophages (MDMs) with HIV for 2 h before addition of uninfected autologous CD4(+) T lymphocytes. Methods: HIV infection was recorded after different time points. Following staining, the measurement of intracellular p24 in the different cell populations was analyzed by flow cytometry. Results: We showed that Langerhans cells/IDCs and macrophages efficiently transferred HIV to CD4(+) T cells. Interestingly, a rapid HIV transfer in trans predominated in MDMs, whereas cis transfer mainly occurred in Langerhans cells/IDC cocultures. Neutralizing antibody 2G12, added to HIV-loaded APCs, efficiently blocked both the trans and the cis infection of T cells. Conclusion: These findings highlight the major contributions of various mucosal cells in HIV dissemination and suggest that HIV hijacks the different properties of APCs to favor its dissemination through the body. They emphasize the role of macrophages in the rapid transmission of HIV to T lymphocytes at mucosal sites, dendritic cells being prone to migration to lymphoid organ for subsequent dissemination by cis transfer.
MeSH term(s)	CD4-Positive T-Lymphocytes/virology ; Cells, Cultured ; Coculture Techniques ; Dendritic Cells/virology ; Flow Cytometry ; HIV Core Protein p24/analysis ; HIV Infections/virology ; HIV-1/isolation & purification ; Humans ; Infant, Newborn ; Macrophages/virology ; Time Factors
Chemical Substances	HIV Core Protein p24
Language	English
Publishing date	2014-03-13
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639076-6
ISSN	1473-5571 ; 0269-9370 ; 1350-2840
ISSN (online)	1473-5571
ISSN	0269-9370 ; 1350-2840
DOI	10.1097/QAD.0000000000000193
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Zs.A 2228: Show issues

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Article: Invasion of endothelial cells by Neisseria meningitidis requires cortactin recruitment by a phosphoinositide-3-kinase/Rac1 signalling pathway triggered by the lipo-oligosaccharide.

Lambotin, Mélanie / Hoffmann, Isabelle / Laran-Chich, Marie-Pierre / Nassif, Xavier / Couraud, Pierre Olivier / Bourdoulous, Sandrine

Journal of cell science

2005 Volume 118, Issue Pt 16, Page(s) 3805–3816

Abstract: Type-IV-pilus-mediated adhesion of Neisseria meningitidis (also known as meningococcus) to human endothelial cells induces the formation of membrane protrusions leading to bacterial uptake. We have previously shown that these protrusions result from a ... ...

Abstract	Type-IV-pilus-mediated adhesion of Neisseria meningitidis (also known as meningococcus) to human endothelial cells induces the formation of membrane protrusions leading to bacterial uptake. We have previously shown that these protrusions result from a Rho- and Cdc42-dependent cortical actin polymerization, and from the activation of the ErbB2 tyrosine-kinase receptor and the Src kinase, leading to tyrosine phosphorylation of cortactin. We report here that N. meningitidis mutants expressing a deglycosylated lipo-oligosaccharide are poorly invasive. These mutants show structurally altered actin polymerization. Moreover, although they efficiently recruit and activate ErbB2 and Src, these mutants are defective in the recruitment and phosphorylation of cortactin. We demonstrate that phosphorylated cortactin controls the cortical actin polymerization, which leads to membrane protrusion formation. In addition, we show that cortactin recruitment is dependent on the activation of a phosphoinositide-3-kinase/Rac1-GTPase signalling pathway, which is required for actin polymerization and internalization of N. meningitidis, and is not activated by the mutant strains. Altogether, these results define a new role for the lipo-oligosaccharide in triggering a phosphoinositide-3-kinase/Rac1 signalling required to elicit an efficient uptake of N. meningitidis in non-phagocytic cells.
MeSH term(s)	Actin Cytoskeleton/metabolism ; Actins/metabolism ; Cell Adhesion/physiology ; Cell Communication/physiology ; Cell Surface Extensions/metabolism ; Cells, Cultured ; Endothelial Cells/metabolism ; Endothelial Cells/microbiology ; Gram-Negative Bacterial Infections/metabolism ; Humans ; Lipopolysaccharides/metabolism ; Mutation/genetics ; Neisseria meningitidis/genetics ; Neisseria meningitidis/physiology ; Phagocytosis/physiology ; Phosphatidylinositol 3-Kinases/metabolism ; Receptor, ErbB-2/metabolism ; Signal Transduction/physiology ; rac1 GTP-Binding Protein/metabolism ; src-Family Kinases/metabolism
Chemical Substances	Actins ; Lipopolysaccharides ; lipid-linked oligosaccharides ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Receptor, ErbB-2 (EC 2.7.10.1) ; src-Family Kinases (EC 2.7.10.2) ; rac1 GTP-Binding Protein (EC 3.6.5.2)
Language	English
Publishing date	2005-08-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2993-2
ISSN	1477-9137 ; 0021-9533
ISSN (online)	1477-9137
ISSN	0021-9533
DOI	10.1242/jcs.02514
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Article ; Online: Neutralizing antibodies inhibit HIV-1 transfer from primary dendritic cells to autologous CD4 T lymphocytes.

Su, Bin / Xu, Ke / Lederle, Alexandre / Peressin, Maryse / Biedma, Marina Elizabeth / Laumond, Géraldine / Schmidt, Sylvie / Decoville, Thomas / Proust, Alizé / Lambotin, Mélanie / Holl, Vincent / Moog, Christiane

Blood

2012 Volume 120, Issue 18, Page(s) 3708–3717

Abstract: Dendritic cells (DCs) support only low levels of HIV-1 replication, but have been shown to transfer infectious viral particles highly efficiently to neighboring permissive CD4 T lymphocytes. This mode of cell-to-cell HIV-1 spread may be a predominant ... ...

Abstract	Dendritic cells (DCs) support only low levels of HIV-1 replication, but have been shown to transfer infectious viral particles highly efficiently to neighboring permissive CD4 T lymphocytes. This mode of cell-to-cell HIV-1 spread may be a predominant mode of infection and dissemination. In the present study, we analyzed the kinetics of fusion, replication, and the ability of HIV-1-specific Abs to inhibit HIV-1 transfer from immature DCs to autologous CD4 T lymphocytes. We found that neutralizing mAbs prevented HIV-1 transfer to CD4 T lymphocytes in trans and in cis, whereas nonneutralizing Abs did not. Neutralizing Abs also significantly decreased HIV-1 replication in DCs, even when added 2 hours after HIV-1 infection. Interestingly, a similar inhibition of HIV-1 replication in DCs was detected with some nonneutralizing Abs and was correlated with DC maturation. We suggest that the binding of HIV-1-specific Abs to FcγRs leads to HIV-1 inhibition in DCs by triggering DC maturation. This efficient inhibition of HIV-1 transfer by Abs highlights the importance of inducing HIV-specific Abs by vaccination directly at the mucosal portal of HIV-1 entry to prevent early dissemination after sexual transmission.
MeSH term(s)	Antibodies, Neutralizing/immunology ; CD4-Positive T-Lymphocytes/immunology ; CD4-Positive T-Lymphocytes/virology ; Cells, Cultured ; Coculture Techniques ; Dendritic Cells/immunology ; Dendritic Cells/virology ; Flow Cytometry ; HIV Infections/transmission ; HIV Infections/virology ; HIV-1/immunology ; Humans
Chemical Substances	Antibodies, Neutralizing
Language	English
Publishing date	2012-09-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood-2012-03-418913
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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

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