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Anti-CD25 Antibody-Mediated Depletion of Effector T Cell Populations Enhances Susceptibility of Mice to Acute but Not Chronic Toxoplasma gondii Infection¹

Kevin N. Couper^2,*, Paula A. Lanthier^*, Georgia Perona-Wright^*, Lawrence W. Kummer^*, Wangxue Chen, Stephen T. Smiley^*, Markus Mohrs^* and Lawrence L. Johnson^*

^* Trudeau Institute, Saranac Lake, NY 12983; and Institute for Biological Sciences, National Research Council of Canada, Ottawa, Ontario, Canada

Natural regulatory T cells (Tregs) constitutively express the IL-2R -chain (CD25) on their surface. Consequently, administration of anti-CD25 Abs is a commonly used technique to deplete Treg populations in vivo. However, activated effector T cells may also transiently express CD25, and are thus also potential targets for anti-CD25 Abs. In this study using Toxoplasma gondii as a model proinflammatory infection, we have examined the capacity of anti-CD25 Abs to target effector T cell populations during an inflammatory episode, to determine to what extent that this action may modulate the outcome of disease. Anti-CD25 Ab-treated C57BL/6 mice displayed significantly reduced CD4⁺ T cell IFN- production during acute T. gondii infection and exhibited reduced weight loss and liver pathology during early acute infection; aspects of infection previously associated with effector CD4⁺ T cell responses. In agreement, anti-CD25 Ab administration impaired parasite control and caused mice to succumb to infection during late acute/early chronic stages of infection with elevated tissue parasite burdens. In contrast, anti-CD25 Ab treatment of mice with established chronic infections did not markedly affect brain parasite burdens, suggesting that protective T cell populations do not express CD25 during chronic stages of T. gondii infection. In summary, we have demonstrated that anti-CD25 Abs may directly abrogate effector T cell responses during an inflammatory episode, highlighting important limitations of the use of anti-CD25 Ab administration to examine Treg function during inflammatory settings.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by a Public Health Service Grant AI061587 from the National Institute of Allergy and Infectious Diseases and by funds provided by the Trudeau Institute.

² Address correspondence and reprint requests to Dr. Kevin N. Couper at the current address: Immunology Unit, Department of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, Keppel Street, London WC1E 7HT, U.K. E-mail address: kevin.couper{at}lshtm.ac.uk

³ Abbreviations used in this paper: Treg, regulatory T cell; yFP, yellow fluorescent protein.

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