{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T20:10:48Z","timestamp":1791231048631,"version":"4.1.0"},"reference-count":33,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2006,8,1]],"date-time":"2006-08-01T00:00:00Z","timestamp":1154390400000},"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":[[2006,8,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Type-I IFNs (IFN-I) provide direct survival signals to T cells during Ag-driven proliferation. Because IFN-I production differs depending on the pathogen, we assessed CD8 T cell requirement for direct IFN-I signals during responses to vaccinia virus (VV), vesicular stomatitis virus (VSV), lymphocytic choriomeningitis virus (LCMV), and Listeria monocytogenes (LM) immunizations in vivo. IFN-I-receptor-deficient (IFN-IR\u00b0) CD8 T cells expanded 3- to 5-fold less and formed a diminished memory pool compared with wild-type (WT) CD8 T cells in response to VV, VSV, or LM. WT CD8 T cells expanded more robustly in response to LCMV-encoded Ags than to Ags encoded by the other three pathogens, and under these conditions the lack of direct IFN-I signals inhibited their expansion by \u223c100-fold. To test whether the high antigenic-load provided by LCMV caused greater expansion and greater IFN-I dependency, we primed WT and IFN-IR\u00b0 OVA-specific OT-1 CD8 T cells with a fixed-number of OVA-peptide-pulsed dendritic cells along with adjuvant effect provided by LCMV, VV, VSV, or LM. Both WT and IFN-IR\u00b0 OT-1 cells were recruited, proliferated, and differentiated into effectors in all the four cases. However, WT OT-1 cells expanded similarly in all four cases. IFN-IR\u00b0 OT-1 cells expanded \u223c20-fold less than the WT OT-1 CD8 T cells when LCMV was used as adjuvant, whereas their expansion was affected only marginally when VV, VSV, or LM were used as adjuvants. Thus, innate\/inflammatory signals induced by different pathogens contribute to CD8 T cell expansion and memory formation via distinct levels of IFN-I dependence.<\/jats:p>","DOI":"10.4049\/jimmunol.177.3.1746","type":"journal-article","created":{"date-parts":[[2014,4,24]],"date-time":"2014-04-24T16:59:02Z","timestamp":1398358742000},"page":"1746-1754","source":"Crossref","is-referenced-by-count":167,"title":["Innate Inflammatory Signals Induced by Various Pathogens Differentially Dictate the IFN-I Dependence of CD8 T Cells for Clonal Expansion and Memory Formation"],"prefix":"10.1093","volume":"177","author":[{"given":"Lucas J","family":"Thompson","sequence":"first","affiliation":[{"name":"Department of Immunology and Washington National Primate Center, University of Washington , 1959 Northeast Pacific Street, Seattle, WA 98195"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ganesh A","family":"Kolumam","sequence":"additional","affiliation":[{"name":"Department of Immunology and Washington National Primate Center, University of Washington , 1959 Northeast Pacific Street, Seattle, WA 98195"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sunil","family":"Thomas","sequence":"additional","affiliation":[{"name":"Department of Immunology and Washington National Primate Center, University of Washington , 1959 Northeast Pacific Street, Seattle, WA 98195"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kaja","family":"Murali-Krishna","sequence":"additional","affiliation":[{"name":"Department of Immunology and Washington National Primate Center, University of Washington , 1959 Northeast Pacific Street, Seattle, WA 98195"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2006,8,1]]},"reference":[{"key":"2025032704042366500_R1","first-page":"6842","volume-title":"J. 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