The Journal of Experimental Medicine
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Published 3 June 2002. doi:10.1084/jem.20011915
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© Rockefeller University Press, 0022-1007/2002/6/1463/ $5.00
The Journal of Experimental Medicine, Volume 195, Number 11, June 3, 2002 1463-1470

Treatment with Soluble Interleukin-15R{alpha} Exacerbates Intracellular Parasitic Infection by Blocking the Development of Memory CD8+ T Cell Response

Imtiaz A. Khan1, Magali Moretto1, Xiao-qing Wei2, Martha Williams1, Joseph D. Schwartzman3 and Foo Y. Liew2

1 Department of Microbiology, Immunology and Parasitology, Louisiana State University Health Science Center, New Orleans, LA 70112
2 Department of Immunology and Bacteriology, University of Glasgow, Glasgow G11 6NT, United Kingdom
3 Department of Pathology, Dartmouth Medical School, Lebanon, NH 03756

Address correspondence to Imtiaz A. Khan, Department of Microbiology, Immunology and Parasitology, Louisiana State University Health Science Center, New Orleans, LA 70112. Phone: 504-568-6116; Fax: 504-568-2918; E-mail: ikhan{at}lsuhsc.edu

Interferon (IFN)-{gamma}–producing CD8+ T cells are important for the successful resolution of the obligate intracellular parasite Toxoplasma gondii by preventing the reactivation or controlling a repeat infection. Previous reports from our laboratory have shown that exogenous interleukin (IL)-15 treatment augments the CD8+ T cell response against the parasite. However, the role of endogenous IL-15 in the proliferation of activated/memory CD8+ T cells during toxoplasma or any other infection is unknown. In this study, we treated T. gondii immune mice with soluble IL-15 receptor {alpha} (sIL-15R{alpha}) to block the host endogenous IL-15. The treatment markedly reduced the ability of the immune animals to control a lethal infection. CD8+ T cell activities in the sIL-15R{alpha}–administered mice were severely reduced as determined by IFN-{gamma} release and target cell lysis assays. The loss of CD8+ T cell immunity due to sIL-15R{alpha} treatment was further demonstrated by adoptive transfer experiments. Naive recipients transferred with CD44hi activated/memory CD8+ T cells and treated with sIL-15R{alpha} failed to resist a lethal T. gondii infection. Moreover, sIL-15R{alpha} treatment of the recipients blocked the ability of donor CD44hi activated/memory CD8+ T cells to replicate in response to T. gondii challenge. To our knowledge, this is the first demonstration of the important role of host IL-15 in the development of antigen-specific memory CD8+ T cells against an intracellular infection.

Key Words: IL-15 • Toxoplasma gondii • IFN-{gamma} • cytotoxic T cells • adoptive transfer


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