{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,11]],"date-time":"2025-11-11T22:00:55Z","timestamp":1762898455248},"reference-count":51,"publisher":"American Society for Microbiology","issue":"5","license":[{"start":{"date-parts":[[2009,5,1]],"date-time":"2009-05-01T00:00:00Z","timestamp":1241136000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2009,5]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>Proinflammatory cytokines, such as gamma interferon (IFN-\u03b3), 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-\u03b3 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\u03b1<jats:sup>\u2212\/\u2212<\/jats:sup>and IL-18<jats:sup>\u2212\/\u2212<\/jats:sup>mice developed frequencies and total numbers of Ag-specific CD8 T cells after<jats:italic>Listeria monocytogenes<\/jats:italic>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\u03b1 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\u03b1; 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\u03b1 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<jats:italic>L. monocytogenes<\/jats:italic>infection.<\/jats:p>","DOI":"10.1128\/iai.01315-08","type":"journal-article","created":{"date-parts":[[2009,2,18]],"date-time":"2009-02-18T03:34:52Z","timestamp":1234928092000},"page":"1894-1903","update-policy":"http:\/\/dx.doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":21,"title":["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<i>Listeria monocytogenes<\/i>Infection"],"prefix":"10.1128","volume":"77","author":[{"given":"Jodie S.","family":"Haring","sequence":"first","affiliation":[{"name":"Department of Microbiology"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"John T.","family":"Harty","sequence":"additional","affiliation":[{"name":"Department of Microbiology"},{"name":"Interdisciplinary Program in Immunology, University of Iowa, Iowa City, Iowa 52242"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1074-7613(00)80596-8"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.immuni.2007.04.013"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-1759(00)00153-8"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.170.10.4933"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1038\/ni1098"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.290.5495.1354"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2004-07-2833"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20020369"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20031051"},{"key":"e_1_3_2_11_2","doi-asserted-by":"crossref","first-page":"299","DOI":"10.4049\/jimmunol.160.1.299","volume":"160","year":"1998","unstructured":"Bohn, E., A. 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