{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T01:52:53Z","timestamp":1791251573321,"version":"4.1.0"},"reference-count":43,"publisher":"American Society for Microbiology","issue":"1","license":[{"start":{"date-parts":[[2008,1,1]],"date-time":"2008-01-01T00:00:00Z","timestamp":1199145600000},"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":["J Virol"],"published-print":{"date-parts":[[2008,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Toll-like receptors (TLRs) and retinoic acid-inducible gene I-like helicases (RLHs) are two major machineries recognizing RNA virus infection of innate immune cells. Intracellular signaling for TLRs and RLHs is mediated by their cytoplasmic adaptors, i.e., MyD88 or TRIF and IPS-1, respectively. In the present study, we investigated the contributions of TLRs and RLHs to the cytotoxic T-lymphocyte (CTL) response by using lymphocytoid choriomeningitis virus (LCMV) as a model virus. The generation of virus-specific cytotoxic T lymphocytes was critically dependent on MyD88 but not on IPS-1. Type I interferons (IFNs) are known to be important for the development of the CTL response to LCMV infection. Serum levels of type I IFNs and proinflammatory cytokines were mainly dependent on the presence of MyD88, although IPS-1\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            mice showed a decrease in IFN-\u03b1 levels but not in IFN-\u03b2 and proinflammatory cytokine levels. Analysis of\n            <jats:italic>Ifna6<\/jats:italic>\n            <jats:sup>+\/GFP<\/jats:sup>\n            reporter mice revealed that plasmacytoid dendritic cells (DCs) are the major source of IFN-\u03b1 in LCMV infection. MyD88\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            mice were highly susceptible to LCMV infection in vivo. These results suggest that recognition of LCMV by plasmacytoid DCs via TLRs is responsible for the production of type I IFNs in vivo. Furthermore, the activation of a MyD88-dependent innate mechanism induces a CTL response, which eventually leads to virus elimination.\n          <\/jats:p>","DOI":"10.1128\/jvi.01640-07","type":"journal-article","created":{"date-parts":[[2007,10,18]],"date-time":"2007-10-18T01:04:48Z","timestamp":1192669488000},"page":"196-206","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":109,"title":["Lymphocytoid Choriomeningitis Virus Activates Plasmacytoid Dendritic Cells and Induces a Cytotoxic T-Cell Response via MyD88"],"prefix":"10.1128","volume":"82","author":[{"given":"Andreas","family":"Jung","sequence":"first","affiliation":[{"name":"Research Institute for Microbial Diseases, Department of Host Defense, Osaka University, Osaka, Japan"},{"name":"Department of Neonatology, Campus Mitte, Charite\u0301-Universitaetsmedizin Berlin, Berlin, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hiroki","family":"Kato","sequence":"additional","affiliation":[{"name":"Research Institute for Microbial Diseases, Department of Host Defense, Osaka University, Osaka, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yutaro","family":"Kumagai","sequence":"additional","affiliation":[{"name":"Research Institute for Microbial Diseases, Department of Host Defense, Osaka University, Osaka, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Himanshu","family":"Kumar","sequence":"additional","affiliation":[{"name":"Research Institute for Microbial Diseases, Department of Host Defense, Osaka University, Osaka, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Taro","family":"Kawai","sequence":"additional","affiliation":[{"name":"Research Institute for Microbial Diseases, Department of Host Defense, Osaka University, Osaka, Japan"},{"name":"ERATO, Japan Science and Technology Agency, Osaka, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Osamu","family":"Takeuchi","sequence":"additional","affiliation":[{"name":"Research Institute for Microbial Diseases, Department of Host Defense, Osaka University, Osaka, Japan"},{"name":"ERATO, Japan Science and Technology Agency, Osaka, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shizuo","family":"Akira","sequence":"additional","affiliation":[{"name":"Research Institute for Microbial Diseases, Department of Host Defense, Osaka University, Osaka, Japan"},{"name":"ERATO, Japan Science and Technology Agency, Osaka, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.176.8.4525"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2006.02.015"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.175.1.196"},{"key":"e_1_3_2_5_2","first-page":"257","volume":"230","year":"2004","unstructured":"Beutler, B. 2004. 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