Skip Navigation


International Immunology Advance Access originally published online on June 23, 2005
International Immunology 2005 17(8):1047-1057; doi:10.1093/intimm/dxh285
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
17/8/1047    most recent
dxh285v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Rogez-Kreuz, C.
Right arrow Articles by Clayette, P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Rogez-Kreuz, C.
Right arrow Articles by Clayette, P.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?


© The Japanese Society for Immunology. 2005. All rights reserved. For permissions, please e-mail: journals.permissions@oupjournals.org

Involvement of IL-6 in the anti-human immunodeficiency virus activity of IFN-{tau} in human macrophages

Christine Rogez-Kreuz1,2, Benjamin Manéglier1,3, Marc Martin1, Nathalie Dereuddre-Bosquet4, Jacques Martal2, Dominique Dormont1,* and Pascal Clayette4

1 Service de Neurovirologie, Commissariat à l'Energie Atomique, Université Paris-Sud, CRSSA, EPHE, IPSC, Fontenay-aux-Roses, France
2 Unité de Biologie du Développement et de la Reproduction, Département de Physiologie Animale, Institut National de la Recherche Agronomique, Jouy-en-Josas, France
3 Unité de Pharmacologie, Département de Biologie, Centre Hospitalier de Versailles, Faculté de Médecine Paris Ile de France Ouest, Le Chesnay, France
4 SPI-BIO, CEA, 18, route du Panorama, B.P.6, 92265 Fontenay-aux-Roses Cedex, France

Correspondence to: P. Clayette; E-mail: pascal.clayette{at}cea.fr

IFN-{tau} is a non-cytotoxic type I IFN responsible for maternal recognition of the foetus in ruminants. IFN-{tau} has been found to inhibit HIV replication more strongly than human IFN-{alpha}, particularly in human monocyte-derived macrophages, without associated toxicity. Ovine IFN-{tau} uses the same anti-viral cellular pathways as human IFN-{alpha} in human macrophages, principally inhibiting the early steps of the biological cycle of HIV, preventing the integration of HIV DNA into the host-cell genome. In this study, we investigated the immunomodulatory properties of IFN-{tau} in human macrophages. We found that IFN-{tau} increased the production of IL-10 and IL-6, but not of IL-1ß or tumour necrosis factor {alpha}, in unstimulated, LPS-stimulated and HIV-1/Ba-L-infected macrophages. We also found that treatment with IL-6 inhibited HIV replication. Moreover, the neutralization of IL-6 activity in the cell culture supernatants of IFN-{tau}-treated macrophages led to a decrease in the anti-retroviral effects of IFN-{tau}, suggesting that IL-6 was involved in the anti-viral activity induced by IFN-{tau}. By focusing on the very early steps of the biological cycle of HIV, we showed that IL-6 co-operated with IFN-{tau} to decrease intracellular HIV RNA levels 2 h after infection.

Keywords: anti-retroviral, HIV, IFN, IFN-{tau}, IL-6, immunomodulation, macrophages

* Dedicated to Professor Dominique Dormont who died in November 2003

Transmitting editor: S. Romagnani


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.