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 Yue, F. Y.
Right arrow Articles by Ostrowski, M. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Yue, F. Y.
Right arrow Articles by Ostrowski, M. A.

 Previous Article  |  Next Article 

Journal of Virology, July 2008, p. 6767-6771, Vol. 82, No. 13
0022-538X/08/$08.00+0     doi:10.1128/JVI.02550-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Virus-Specific Interleukin-17-Producing CD4+ T Cells Are Detectable in Early Human Immunodeficiency Virus Type 1 Infection {triangledown}

Feng Yun Yue,1 Asad Merchant,1 Colin M. Kovacs,2 Mona Loutfy,2 Desmond Persad,2 and Mario A. Ostrowski1,3*

Clinical Sciences Division, University of Toronto, Toronto, Canada,1 St. Michael's Hospital, University of Toronto, Toronto, Canada,3 CIRC (Canadian Immunodeficiency Research Collaborative), Toronto, Canada2

Received 28 November 2007/ Accepted 11 April 2008

TH-17 cells have been shown to play a role in bacterial defense, acute inflammation, and autoimmunity. We examined the role of interleukin 17 (IL-17) production in human immunodeficiency virus type 1 (HIV-1) infection. Both HIV-1- and cytomegalovirus (CMV)-specific IL-17-producing CD4+ T cells were detectable in early HIV-1 infection but were reduced to nondetectable levels in chronic and nonprogressive HIV-1 infection. IL-17-producing CMV-specific cells were not detected in blood from HIV-1-uninfected normal volunteers. Virus-specific TH-17 cells could coexpress other cytokines and could express CCR4 or CXCR3. Although the etiology of these cells has yet to be established, we propose that microbial translocation may induce them.

* Corresponding author. Mailing address: University of Toronto, Clinical Sciences Division, Rm. 6271, Medical Sciences Building, Toronto, ON, Canada M5S 1A8. Phone: (416) 946-5805. Fax: (416) 978-8765. E-mail: mario.ostrowski{at}gmail.com

{triangledown} Published ahead of print on 23 April 2008.

Journal of Virology, July 2008, p. 6767-6771, Vol. 82, No. 13
0022-538X/08/$08.00+0     doi:10.1128/JVI.02550-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Hou, W., Kang, H. S., Kim, B. S. (2009). Th17 cells enhance viral persistence and inhibit T cell cytotoxicity in a model of chronic virus infection. JEM 206: 313-328 [Abstract] [Full Text]  
  • Pirofski, L.-a., Casadevall, A. (2009). Rethinking T cell immunity in oropharyngeal candidiasis. JEM 206: 269-273 [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»