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Inhibition of IL-2 Induced IL-10 Production as a Principle of Phase-Specific Immunotherapy¹

National Centre for Cell Science, Ganeshkhind, Maharashtra, India

Leishmania donovani, a protozoan parasite, inflicts a fatal disease, visceral leishmaniasis. The suppression of antileishmanial T cell responses that characterizes the disease was proposed to be due to deficiency of a T cell growth factor, IL-2. We demonstrate that during the first week after L. donovani infection, IL-2 induces IL-10 that suppresses the host-protective functions of T cells 14 days after infection. The observed suppression is concurrent with increased CD4⁺glucocorticoid-induced TNF receptor⁺ T cells and Foxp3 expression in BALB/c mice, implicating IL-2-dependent regulatory T cell control of antileishmanial immune responses. Indeed, IL-2 and IL-10 neutralization at different time points after the infection demonstrates their distinct roles at the priming and effector phases, respectively, and establishes kinetic modulation of ongoing immune responses as a principle of a rational, phase-specific immunotherapy.

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 Council for Scientific and Industrial Research and Department of Biotechnology grants (to M.B., A.A., S.M., and R.K.).

² M.B. and N.J. contributed equally to this work.

³ Address correspondence and reprint requests to Dr. Bhaskar Saha, National Centre for Cell Science, Ganeshkhind, Pune 411 007, India. E-mail address: sahab{at}nccs.res.in

⁴ Abbreviations used in this paper: GITR, glucocorticoid-induced TNF receptor; CSA, crude soluble Ag; DTH, delayed-type hypersensitivity; t-reg, regulatory T.

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