Skip Navigation


International Immunology Advance Access originally published online on June 3, 2005
International Immunology 2005 17(6):729-736; doi:10.1093/intimm/dxh252
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
17/6/729    most recent
dxh252v1
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 arrow Search for citing articles in:
ISI Web of Science (6)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Ji, J.
Right arrow Articles by Cloyd, M. W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ji, J.
Right arrow Articles by Cloyd, M. W.
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

HIV-1 induces IL-10 production in human monocytes via a CD4-independent pathway

Jiaxiang Ji, Gautam K. Sahu, Vivian L. Braciale and Miles W. Cloyd

Department of Microbiology and Immunology, University of Texas Medical Branch at Galveston, Galveston, TX 77555-1070, USA

Correspondence to: M. W. Cloyd; E-mail: mcloyd{at}utmb.edu

In HIV-infected patients, increased levels of IL-10, mainly produced by virally infected monocytes, were reported to be associated with impaired cell-mediated immune responses. In this study, we investigated how HIV-1 induces IL-10 production in human monocytes. We found that CD14+ monocytes infected by either HIV-1213 (X4) or HIV-1BaL (R5) produced IL-10, IL-6, tumor necrosis factor-{alpha} (TNF-{alpha}), and to a lesser extent, IFN-{gamma}. However, the capacity of HIV-1 to induce these cytokines was not dependent on virus replication since UV-inactivated HIV-1 induced similar levels of these cytokines. In addition, soluble HIV-1 gp160 could induce CD14+ monocytes to produce IL-10 but at lower levels. Cross-linking CD4 molecules (XLCD4) with anti-CD4 mAbs and goat anti-mouse IgG (GAM) resulted in high levels of IL-6, TNF-{alpha} and IFN-{gamma} but no IL-10 production by CD14+ monocytes. Interestingly, neither anti-CD4 mAbs nor recombinant soluble CD4 (sCD4) receptor could block IL-10 secretion induced by HIV-1213, HIV-1BaL or HIV-1 gp160 in CD14+ monocytes, whereas anti-CD4 mAb or sCD4 almost completely blocked the secretion of the other cytokines. Furthermore, HIV-1213 could induce IL-10 mRNA expression in CD14+ monocytes while XLCD4 by anti-CD4 mAb and GAM failed to do so. As with IL-10 protein levels, HIV-1213-induced IL-10 mRNA expression in CD14+ monocytes could not be inhibited by anti-CD4 mAb or sCD4. Taken together, HIV-1 binding to CD14+ monocytes can induce CD4-independent IL-10 production at both mRNA and protein levels. This finding suggests that HIV induces the immunosuppressive IL-10 production in monocytes and is not dependent on CD4 molecules and that interference with HIV entry through CD4 molecules may have no impact on counteracting the effects of IL-10 during HIV infection.

Keywords: CD4-independent, HIV-1, IL-10, monocytes

Transmitting editor: R. Steinman


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


This article has been cited by other articles:


Home page
 J. Immunol.Home page
K. N. Couper, D. G. Blount, and E. M. Riley
IL-10: The Master Regulator of Immunity to Infection
J. Immunol., May 1, 2008; 180(9): 5771 - 5777.
[Abstract] [Full Text] [PDF]


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.