{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,11]],"date-time":"2026-04-11T05:41:09Z","timestamp":1775886069250,"version":"3.50.1"},"reference-count":65,"publisher":"Oxford University Press (OUP)","issue":"11","license":[{"start":{"date-parts":[[2017,12,1]],"date-time":"2017-12-01T00:00:00Z","timestamp":1512086400000},"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":[[2017,12,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Type III IFNs are important mediators of antiviral immunity. IFN-\u03bb4 is a unique type III IFN because it is produced only in individuals who carry a dG allele of a genetic variant rs368234815-dG\/TT. Counterintuitively, those individuals who can produce IFN-\u03bb4, an antiviral cytokine, are also less likely to clear hepatitis C virus infection. In this study, we searched for unique functional properties of IFN-\u03bb4 that might explain its negative effect on hepatitis C virus clearance. We used fresh primary human hepatocytes (PHHs) treated with recombinant type III IFNs or infected with Sendai virus to model acute viral infection and subsequently validated our findings in HepG2 cell line models. Endogenous IFN-\u03bb4 protein was detectable only in Sendai virus\u2013infected PHHs from individuals with the dG allele, where it was poorly secreted but highly functional, even at concentrations &amp;lt; 50 pg\/ml. IFN-\u03bb4 acted faster than other type III IFNs in inducing antiviral genes, as well as negative regulators of the IFN response, such as USP18 and SOCS1. Transient treatment of PHHs with IFN-\u03bb4, but not IFN-\u03bb3, caused a strong and sustained induction of SOCS1 and refractoriness to further stimulation with IFN-\u03bb3. Our results suggest unique functional properties of IFN-\u03bb4 that can be important in viral clearance and other clinical conditions.<\/jats:p>","DOI":"10.4049\/jimmunol.1700807","type":"journal-article","created":{"date-parts":[[2017,10,25]],"date-time":"2017-10-25T16:13:01Z","timestamp":1508947981000},"page":"3808-3820","source":"Crossref","is-referenced-by-count":55,"title":["IFN-\u03bb4 Attenuates Antiviral Responses by Enhancing Negative Regulation of IFN Signaling"],"prefix":"10.1093","volume":"199","author":[{"given":"Adeola A","family":"Obajemu","sequence":"first","affiliation":[{"name":"Laboratory of Translational Genomics, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health , Bethesda, MD 20892"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nina","family":"Rao","sequence":"additional","affiliation":[{"name":"Laboratory of Translational Genomics, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health , Bethesda, MD 20892"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kari A","family":"Dilley","sequence":"additional","affiliation":[{"name":"Virology Group, J. Craig Venter Institute , Rockville, MD 20850"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Joselin M","family":"Vargas","sequence":"additional","affiliation":[{"name":"Laboratory of Translational Genomics, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health , Bethesda, MD 20892"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Faruk","family":"Sheikh","sequence":"additional","affiliation":[{"name":"Office of Biotechnology Products, Center for Drug Evaluation and Research, U.S. Food and Drug Administration , Silver Spring, MD 20993"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0695-5276","authenticated-orcid":false,"given":"Raymond P","family":"Donnelly","sequence":"additional","affiliation":[{"name":"Office of Biotechnology Products, Center for Drug Evaluation and Research, U.S. Food and Drug Administration , Silver Spring, MD 20993"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Reed S","family":"Shabman","sequence":"additional","affiliation":[{"name":"Virology Group, J. Craig Venter Institute , Rockville, MD 20850"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5240-7115","authenticated-orcid":false,"given":"Eric G","family":"Meissner","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases, Department of Microbiology and Immunology, Medical University of South Carolina , Charleston, SC 29425"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9622-2091","authenticated-orcid":false,"given":"Ludmila","family":"Prokunina-Olsson","sequence":"additional","affiliation":[{"name":"Laboratory of Translational Genomics, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health , Bethesda, MD 20892"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6342-2380","authenticated-orcid":false,"given":"Olusegun O","family":"Onabajo","sequence":"additional","affiliation":[{"name":"Laboratory of Translational Genomics, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health , Bethesda, MD 20892"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2017,12,1]]},"reference":[{"key":"2025030614531654000_r1","doi-asserted-by":"crossref","first-page":"164","DOI":"10.1038\/ng.2521","article-title":"A variant upstream of IFNL3 (IL28B) creating a new interferon gene IFNL4 is associated with impaired clearance of hepatitis C virus","volume":"45","author":"Prokunina-Olsson","year":"2013","journal-title":"Nat. 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