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Th17 cells and regulatory T cells in elite control over HIV and SIV

Hartigan-O'Connor, Dennis Ja; Hirao, Lauren Ab; McCune, Joseph Ma,*; Dandekar, Satyab,*

Current Opinion in HIV and AIDS: May 2011 - Volume 6 - Issue 3 - p 221–227
doi: 10.1097/COH.0b013e32834577b3
Elite controllers: Edited by Steven G. Deeks, Alexandre Harari and Joel Blankson

Purpose of review We present current findings about two subsets of CD4+ T cells that play an important part in the initial host response to infection with the HIV type 1: those producing IL-17 (Th17 cells) and those with immunosuppressive function (CD25+FoxP3+ regulatory T cells or T-reg). The role of these cells in the control of viral infection and immune activation as well as in the prevention of immune deficiency in HIV-infected elite controllers will be examined. We will also discuss the use of the simian immunodeficiency virus (SIV)-infected macaque model of AIDS to study the interplay between these cells and lentiviral infection in vivo.

Recent findings Study of Th17 cells in humans and nonhuman primates (NHPs) has shown that depletion of these cells is associated with the dissemination of microbial products from the infected gut, increased systemic immune activation, and disease progression. Most impressively, having a smaller Th17-cell compartment has been found to predict these outcomes. T-reg have been associated with the reduced antiviral T-cell responses but not with the suppression of generalized T cell activation. Both cell subsets influence innate immune responses and, in doing so, may shape the inflammatory milieu of the host at infection.

Summary Interactions between Th17 cells, T-reg, and cells of the innate immune system influence the course of HIV and SIV infection from its earliest stages, even before the appearance of adaptive immunity. Such interactions may be pivotal for elite control over disease progression.

aDivision of Experimental Medicine, Department of Medicine, University of California, San Francisco, USA

bDepartment of Medical Microbiology and Immunology, School of Medicine, University of California at Davis, Davis, California, USA

*Joseph M. McCune and Satya Dandekar contributed equally to the writing of this article.

Correspondence to Dennis J. Hartigan-O'Connor, Division of Experimental Medicine, University of California, Box 1234, San Francisco, CA 94110, USA Tel: +1 415 206 8113; fax: +1 415 206 8091; e-mail: dhartigan@medsfgh.ucsf.edu

© 2011 Lippincott Williams & Wilkins, Inc.