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Blood, 1 October 2008, Vol. 112, No. 7, pp. 2858-2868.
Prepublished online as a Blood First Edition Paper on June 10, 2008; DOI 10.1182/blood-2008-03-145946.
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Submitted March 17, 2008
Accepted May 27, 2008
FoxP3+CD4+ Treg cells play an important role in acute HIV-1 infection in humanized rag2-/- C-/- mice in vivo
Qi Jiang, Liguo Zhang, Rui Wang, Jerry Jeffrey, Michael L Washburn, Dedeke Brouwer, Selena Barbour, Grigoriy I Kovalev, Derya Unutmaz, and Lishan Su*
Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States
Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States
Department of Microbiology, New York University School of Medicine, New York, NY, United States
Curriculum in Genetics and Molecular Biology, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States
* Corresponding author; email: lsu{at}med.unc.edu.
The role of FoxP3+CD4+ regulatory T (Treg) cells in HIV-1 disease in vivo is poorly understood due to the lack of a robust model. We report here that CD4+FoxP3+ T cells are developed in all lymphoid organs in humanized rag2-/- C-/- (DKO-hu HSC) mice and they display both Treg phenotype and function. These FoxP3+ Treg cells are preferentially infected and depleted by a pathogenic HIV-1 isolate in HIV-infected DKO-hu HSC mice; and depletion of Treg cells is correlated with induction of their apoptosis in vivo. When CD4+CD25+/hi Treg cells are depleted with the IL2-toxin fusion protein (ONTAK), HIV-1 infection is significantly impaired. This is demonstrated by reduced levels of productively infected cells in lymphoid organs and lower plasma viremia. Therefore, FoxP3+ Treg cells are productively infected and play an important role in acute HIV-1 infection in vivo. The DKO-hu HSC mouse will be a valuable model to study human Treg functions and their role in HIV-1 pathogenesis in vivo.
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