{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,27]],"date-time":"2026-10-27T07:16:34Z","timestamp":1793085394629,"version":"4.5.0"},"reference-count":27,"publisher":"Oxford University Press (OUP)","issue":"11","license":[{"start":{"date-parts":[[2006,12,1]],"date-time":"2006-12-01T00:00:00Z","timestamp":1164931200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2006,12,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Cytokines are critical determinants for specification of lineage-defining transcription factors of CD4+ T cell subsets. Little is known, however, about how cytokines regulate expression of T-bet and eomesodermin (Eomes) in effector and memory CD8+ T cells. We now report that IL-12, a signature of cell-mediated immunity, represses Eomes while positively regulating T-bet in effector CD8+ T cells during infection with Listeria monocytogenes. After resolution of infection and abatement of IL-12 signaling, Eomes expression rises whereas T-bet expression declines in memory CD8+ T cells. Eomes becomes derepressed in effector cells by ablation of IL-12 signaling. In the absence of IL-12, the dynamics of clonal expansion and contraction are also perturbed. Together, these results reveal how a pathogen-associated signal, such as IL-12, could act as a switch, regulating appropriate clonal growth and decline while, in parallel, shaping a unique pattern of fate-determining transcription factors.<\/jats:p>","DOI":"10.4049\/jimmunol.177.11.7515","type":"journal-article","created":{"date-parts":[[2014,4,18]],"date-time":"2014-04-18T13:14:46Z","timestamp":1397826886000},"page":"7515-7519","source":"Crossref","is-referenced-by-count":297,"title":["Cutting Edge: IL-12 Inversely Regulates T-bet and Eomesodermin Expression during Pathogen-Induced CD8+ T Cell Differentiation"],"prefix":"10.1093","volume":"177","author":[{"given":"Naofumi","family":"Takemoto","sequence":"first","affiliation":[{"name":"Abramson Family Cancer Research Institute and Department of Medicine, University of Pennsylvania , Philadelphia, PA 19104"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrew M","family":"Intlekofer","sequence":"additional","affiliation":[{"name":"Abramson Family Cancer Research Institute and Department of Medicine, University of Pennsylvania , Philadelphia, PA 19104"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John T","family":"Northrup","sequence":"additional","affiliation":[{"name":"Abramson Family Cancer Research Institute and Department of Medicine, University of Pennsylvania , Philadelphia, PA 19104"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"E John","family":"Wherry","sequence":"additional","affiliation":[{"name":"The Wistar Institute , Philadelphia, PA 19104"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Steven L","family":"Reiner","sequence":"additional","affiliation":[{"name":"Abramson Family Cancer Research Institute and Department of Medicine, University of Pennsylvania , Philadelphia, PA 19104"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2006,12,1]]},"reference":[{"key":"2026012810555720800_R1","first-page":"655","volume-title":"Cell","year":"2000"},{"key":"2026012810555720800_R2","first-page":"1907","volume-title":"Science","year":"2001"},{"key":"2026012810555720800_R3","first-page":"338","volume-title":"Science","year":"2002"},{"key":"2026012810555720800_R4","first-page":"15818","volume-title":"Proc. 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