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Blood, 1 December 2006, Vol. 108, No. 12, pp. 3808-3817.
Prepublished online as a Blood First Edition Paper on August 10, 2006; DOI 10.1182/blood-2006-05-021576.
 Previous Article | Next Article 
Submitted May 8, 2006
Accepted July 21, 2006
HIV-1 driven regulatory T cell accumulation in lymphoid tissues is associated with disease progression in HIV/AIDS
Jakob Nilsson, Adriano Boasso, Paula A Velilla, Rui Zhang, Monica Vaccari, Genoveffa Franchini, Gene M Shearer, Jan Andersson, and Claire Chougnet*
Center for Infectious Medicine, Division of Infectious Diseases, Karolinska Institute, Sweden
Experimental Immunology Branch, National Cancer Institute, NIH, Bethesda, MD, USA
Division of Molecular Immunology, Cincinnati Children's Hospital Research Foundation, Ohio, USA
Division of Molecular Immunology, Cincinnati Chi, Cincinnati Children's Hospital Research Foundation
Animal Models and Retroviral Vaccines Section, National Cancer Institute, Bethesda, MD, USA
* Corresponding author; email: choqj6{at}cchmc.org.
Regulatory T cells (Treg) accumulate in the lymphoid tissues of HIV-infected individuals, contributing to the inability of the immune system to control virus replication. We investigate here Treg numbers and functional markers (FOXP3, CTLA-4, IDO and TGF- 1) in lymphoid tissues from untreated infected hosts with progressive or non-progressive disease (HIV-infected humans and SIV-infected macaques). We found that increased numbers FOXP3+ T cells as well as increased expression of Treg-associated functional markers were detected only during progressive disease, and such increases were not correlated with immune activation. Importantly, a high perforin/FOXP3 ratio was associated with non-progressive disease, suggesting that the immune control of virus replication represents a balance between cell-mediated immune responses and Treg-mediated counter-regulation of such responses. Furthermore, using an in vitro model of Treg-HIV interactions, we showed that exposure of Treg to HIV selectively promoted their survival via a CD4-gp120 dependent pathway, thus providing an underlying mechanism for the accumulation of Treg in infected hosts with active viral replication. Considered together, our findings imply that therapeutic manipulation of Treg number and/or function could improve immune control of HIV infection.
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