Volume 2012, Issue 1 908314
Review Article
Open Access

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

Mohammad-Ali Jenabian

Mohammad-Ali Jenabian

Chronic Viral Illnesses Service, McGill University Health Centre, 3650 St. Urbain Street, Montreal, QC, Canada H2X 2P4, muhc.ca

Research Institute, McGill University Health Centre, Montreal, QC, Canada H3H 2R9, muhc.ca

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Petronela Ancuta

Petronela Ancuta

Department of Microbiology and Immunology, Faculty of Medicine, University of Montreal, Montreal, QC, Canada H3T 1J4, umontreal.ca

CHUM Research Center, Saint-Luc Hospital, Montreal, QC, Canada H2X 1P1, chumtl.qc.ca

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Norbert Gilmore

Norbert Gilmore

Chronic Viral Illnesses Service, McGill University Health Centre, 3650 St. Urbain Street, Montreal, QC, Canada H2X 2P4, muhc.ca

Research Institute, McGill University Health Centre, Montreal, QC, Canada H3H 2R9, muhc.ca

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Jean-Pierre Routy

Corresponding Author

Jean-Pierre Routy

Chronic Viral Illnesses Service, McGill University Health Centre, 3650 St. Urbain Street, Montreal, QC, Canada H2X 2P4, muhc.ca

Research Institute, McGill University Health Centre, Montreal, QC, Canada H3H 2R9, muhc.ca

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First published: 2012
Citations: 34
Academic Editor: Bapi Pahar

Abstract

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.

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