Table of Contents Author Guidelines Submit a Manuscript
Clinical and Developmental Immunology
Volume 2012, Article ID 908314, 12 pages
Review Article

Regulatory T Cells in HIV Infection: Can Immunotherapy Regulate the Regulator?

1Chronic Viral Illnesses Service, McGill University Health Centre, 3650 St. Urbain Street, Montreal, QC, Canada H2X 2P4
2Research Institute, McGill University Health Centre, Montreal, QC, Canada H3H 2R9
3Department of Microbiology and Immunology, Faculty of Medicine, University of Montreal, Montreal, QC, Canada H3T 1J4
4CHUM Research Center, Saint-Luc Hospital, Montreal, QC, Canada H2X 1P1

Received 16 July 2012; Accepted 28 August 2012

Academic Editor: Bapi Pahar

Copyright © 2012 Mohammad-Ali Jenabian et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Regulatory T cells (Tregs) have a dominant role in self-tolerance and control of autoimmune diseases. These cells also play a pivotal role in chronic viral infections and cancer by limiting immune activation and specific immune response. The role of Tregs in HIV pathogenesis remains poorly understood as their function, changes according to the phases of infection. Tregs can suppress anti-HIV specific responses and conversely can have a beneficial role by reducing the deleterious impact of immune activation. We review the frequency, function and homing potential of Tregs in the blood and lymphoid tissues as well as their interaction with dendritic cells in the context of HIV infection. We also examine the new insights generated by recombinant IL-2 and IL-7 clinical trials in HIV-infected adults, including the immunomodulatory effects of Tregs. Based on their detrimental role in limiting anti-HIV responses, we propose Tregs as potential targets for immunotherapeutic strategies aimed at decreasing Tregs frequency and/or immunosuppressive function. However, such approaches require a better understanding of the time upon infection when interfering with Treg function may not cause a deleterious state of hyperimmune activation.