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Infect. Immun. doi:10.1128/IAI.01500-06
Copyright (c) 2006, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Endogenous CD4+CD25+ Regulatory T Cells Have Limited Role in Control of Trypanosoma cruzi Infection in Mice

Center for Tropical and Emerging Global Diseases and Department of Cellular Biology, University of Georgia. Athens, GA, 30602

^* To whom correspondence should be addressed. Email: Tarleton{at}cb.uga.edu.

	Abstract

Infection with the protozoan parasite Trypanosoma cruzi results in a robust and multi-faceted immune response that controls parasite load, but is unable to completely clear infection, resulting in parasite persistence and a chronic illness known as Chagas disease in humans. The severity of Chagas disease is correlated with persistent parasitism of muscle, neuronal, and gut tissues. The natural immunomodulatory function of endogenous CD4+CD25+ regulatory T cells (Treg) to limit hyperactive immune responses may be exploited by microbes to persist despite host responses. In this study, we show that Treg are not necessary for T. cruzi evasion of immune responses during acute or chronic infection. In vivo anti-CD25 monoclonal antibody mediated depletion of Treg from mice prior to challenge with a lethal strain, or prior to and during acute infection with a non-lethal strain of parasite, neither improved nor worsened the outcome of immune responses: differences in parasitemia, kinetics of antigen-specific CD8+ T cell expansion, and CD8+ T cell effector function (both in vivo and ex vivo) were of similar magnitude in both depleted and control groups. Furthermore, depletion of CD25+ cells from chronically-infected mice did not enhance immune responses of muscle-derived CD8+ T cells, nor could FoxP3 mRNA/scurfin-expressing leukocytes be isolated from muscle tissue. Based on the results of this study, it is concluded that Treg do not appear to play a major role in regulating CD8+ T cell effector responses during the acute phase of infection, nor in the muscle of mice during chronic T. cruzi infection.

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