| PMID : |
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(17056559) |
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| titre : |
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The engagement of activating FcgammaRs inhibits primate lentivirus replication in human macrophages. |
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| auteur(s) : |
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Annie David1, Asier Sáez-Cirión1, Pierre Versmisse1, Odile Malbec2, Bruno Iannascoli2, Florence Herschke1, Marianne Lucas3, Françoise Barré-Sinoussi1, Jean-François Mouscadet4, Marc Daëron2, Gianfranco Pancino ( ) 1 |
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| laboratoire : |
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| résumé : |
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We previously reported that the stimulation of monocyte-derived macrophages (MDM) by plate-bound i.v. Igs inhibits HIV-1 replication. In this study, we show that IgG immune complexes also suppress HIV-1 replication in MDMs and that activating receptors for the Fc portion of IgG-FcgammaRI, FcgammaRIIA, and FcgammaRIII-are responsible for the inhibition. MDM stimulation through FcgammaRs induces activation signals and the secretion of HIV-1 modulatory cytokines, such as M-CSF, TNF-alpha, and macrophage-derived chemokine. However, none of these cytokines contribute to HIV-1 suppression. HIV-1 entry and postintegration steps of viral replication are not affected, whereas reduced levels of reverse transcription products and of integrated proviruses, as determined by real-time PCR analysis, account for the suppression of HIV-1 gene expression in FcgammaR-activated MDMs. We found that FcgammaR-dependent activation of MDMs also inhibits the replication of HIV-2, SIVmac, and SIVagm, suggesting a common control mechanism for primate immunodeficiency lentiviruses in activated macrophages. |
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| domaine : |
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Sciences du Vivant/Médecine humaine et pathologie/Maladies infectieuses
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langue du texte intégral : |
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Anglais |
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| ISSN : |
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0022-1767 |
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| type de publication : |
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Articles dans des revues avec comité de lecture |
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| journal : |
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| Journal of Immunology (J Immunol) |
| Publisher |
American Association of Immunologists |
| ISSN |
0022-1767 |
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| Audience : |
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non spécifiée |
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| date de publication : |
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01/11/2006 |
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| volume : |
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177 |
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| numéro : |
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9 |
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| page, identifiant, ... : |
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6291-300 |
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| Descripteur(s) MeSH : |
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Animals – Cells – Cultured – DNA – Complementary – Viral – HIV-1 – Humans – Lentivirus – Macrophage Activation – Macrophages – Primates – Proviruses – Receptors – IgG – Virus Replication |
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