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Infection and Immunity, May 2009, p. 1894-1903, Vol. 77, No. 5
0019-9567/09/$08.00+0     doi:10.1128/IAI.01315-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Interleukin-18-Related Genes Are Induced during the Contraction Phase but Do Not Play Major Roles in Regulating the Dynamics or Function of the T-Cell Response to Listeria monocytogenes Infection{triangledown}

Jodie S. Haring1 and John T. Harty1,2*

Department of Microbiology,1 Interdisciplinary Program in Immunology, University of Iowa, Iowa City, Iowa 522422

Received 28 October 2008/ Returned for modification 4 January 2009/ Accepted 5 February 2009

Proinflammatory cytokines, such as gamma interferon (IFN-{gamma}), impact aspects of T-cell responses after infection, including expansion, contraction, and memory formation. Interleukin-18 (IL-18) functions as a proinflammatory cytokine by stimulating the production of IFN-{gamma} from multiple cell types and accentuating the development of Th1 CD4 T-cell responses. Focused microarray analyses revealed upregulation of IL-18 and IL-18 receptor genes in CD8 T cells during the contraction phase. Based on these findings we investigated if and how signaling through the IL-18 receptor influences the development and kinetics of antigen (Ag)-specific CD8 and CD4 T-cell responses following infection. IL-18R{alpha}–/– and IL-18–/– mice developed frequencies and total numbers of Ag-specific CD8 T cells after Listeria monocytogenes infection that were similar to those of wild-type C57BL/6 mice. The kinetics of expansion, contraction, and memory CD8 T-cell maintenance were also similar. When IL-18R{alpha} deficiency was isolated to Ag-specific CD8 T cells, the kinetics of the expansion and contraction phases were also normal. These basic findings were confirmed by examining the response to vaccinia virus infection. In contrast, the expansion of Ag-specific CD4 T cells was slightly curtailed by the absence of IL-18R{alpha}; however, contraction and the maintenance of memory were not altered. Importantly, both memory Ag-specific CD8 and CD4 T cells generated in the absence of IL-18R{alpha} expanded appropriately after secondary antigen exposure and were protective, indicating that signaling through the IL-18 receptor is not required for normal T-cell response kinetics and survival of immunized mice challenged with a lethal L. monocytogenes infection.

* Corresponding author. Mailing address: Department of Microbiology, 3-512 BSB, University of Iowa, 51 Newton Road, Iowa City, IA 52242. Phone: (319) 335-9720. Fax: (319) 335-9006. E-mail: john-harty{at}uiowa.edu

{triangledown} Published ahead of print on 17 February 2009.

Editor: J. L. Flynn

Infection and Immunity, May 2009, p. 1894-1903, Vol. 77, No. 5
0019-9567/09/$08.00+0     doi:10.1128/IAI.01315-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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