This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Spencer, J. V.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Spencer, J. V.

 Previous Article  |  Next Article 

Journal of Virology, February 2007, p. 2083-2086, Vol. 81, No. 4
0022-538X/07/$08.00+0     doi:10.1128/JVI.01655-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

The Cytomegalovirus Homolog of Interleukin-10 Requires Phosphatidylinositol 3-Kinase Activity for Inhibition of Cytokine Synthesis in Monocytes{triangledown}

Juliet V. Spencer*

Department of Biology, University of San Francisco, San Francisco, California 94117

Received 1 August 2006/ Accepted 13 November 2006

Human cytomegalovirus (CMV) has evolved numerous strategies for evading host immune defenses, including piracy of cellular cytokines. A viral homolog of interleukin-10, designated cmvIL-10, binds to the cellular IL-10 receptor and effects potent immune suppression. The signaling pathways employed by cmvIL-10 were investigated, and the classic IL-10R/JAK1/Stat3 pathway was found to be activated in monocytes. However, inhibition of JAK1 had little effect on cmvIL-10-mediated suppression of tumor necrosis factor alpha (TNF-{alpha}) production. Inhibition of the phosphatidylinositol 3-kinase/Akt pathway had a more significant impact on TNF-{alpha} levels but did not completely relieve the immune suppression, demonstrating that cmvIL-10 stimulates multiple signaling pathways to modulate cell function.

* Mailing address: Department of Biology, University of San Francisco, 2130 Fulton St., San Francisco, CA 94117. Phone: (415) 422-5470. Fax: (415) 422-6363. E-mail: jspencer{at}usfca.edu.

{triangledown} Published ahead of print on 22 November 2006.

Journal of Virology, February 2007, p. 2083-2086, Vol. 81, No. 4
0022-538X/07/$08.00+0     doi:10.1128/JVI.01655-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Carter, C.J. (2009). Schizophrenia Susceptibility Genes Directly Implicated in the Life Cycles of Pathogens: Cytomegalovirus, Influenza, Herpes simplex, Rubella, and Toxoplasma gondii. Schizophr Bull 35: 1163-1182 [Abstract] [Full Text]  
  • Slobedman, B., Barry, P. A., Spencer, J. V., Avdic, S., Abendroth, A. (2009). Virus-Encoded Homologs of Cellular Interleukin-10 and Their Control of Host Immune Function. J. Virol. 83: 9618-9629 [Full Text]  
  • Sloan, D. D., Jerome, K. R. (2007). Herpes Simplex Virus Remodels T-Cell Receptor Signaling, Resulting in p38-Dependent Selective Synthesis of Interleukin-10. J. Virol. 81: 12504-12514 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»