{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,10]],"date-time":"2026-06-10T17:02:35Z","timestamp":1781110955987,"version":"3.54.1"},"reference-count":34,"publisher":"National Academy of Sciences","issue":"52","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2008,12,30]]},"abstract":"<jats:p>\n                    Type I IFNs were discovered as the primary antiviral cytokines and are now known to serve critical functions in host defense against bacterial pathogens. Accordingly, established mediators of IFN antiviral activity may mediate previously unrecognized antibacterial functions. RNase-L is the terminal component of an RNA decay pathway that is an important mediator of IFN-induced antiviral activity. Here, we identify a role for RNase-L in the host antibacterial response. RNase-L\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice exhibited a dramatic increase in mortality after challenge with\n                    <jats:italic>Bacillus anthracis<\/jats:italic>\n                    and\n                    <jats:italic>Escherichia coli<\/jats:italic>\n                    ; this increased susceptibility was due to a compromised immune response resulting in increased bacterial load. Investigation of the mechanisms of RNase-L antibacterial activity indicated that RNase-L is required for the optimal induction of proinflammatory cytokines that play essential roles in host defense from bacterial pathogens. RNase-L also regulated the expression of the endolysosomal protease, cathepsin-E, and endosome-associated activities, that function to eliminate internalized bacteria and may contribute to RNase-L antimicrobial action. Our results reveal a unique role for RNase-L in the antibacterial response that is mediated through multiple mechanisms. As a regulator of fundamental components of the innate immune response, RNase-L represents a viable therapeutic target to augment host defense against diverse microbial pathogens.\n                  <\/jats:p>","DOI":"10.1073\/pnas.0807265105","type":"journal-article","created":{"date-parts":[[2008,12,15]],"date-time":"2008-12-15T21:42:10Z","timestamp":1229377330000},"page":"20816-20821","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":58,"title":["An essential role for the antiviral endoribonuclease, RNase-L, in antibacterial immunity"],"prefix":"10.1073","volume":"105","author":[{"given":"Xiao-Ling","family":"Li","sequence":"first","affiliation":[{"name":"Graduate Program in Molecular Medicine,"},{"name":"Marlene and Stewart Greenebaum Cancer Center,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Heather J.","family":"Ezelle","sequence":"additional","affiliation":[{"name":"Marlene and Stewart Greenebaum Cancer Center,"},{"name":"Department of Microbiology and Immunology,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tae-Jin","family":"Kang","sequence":"additional","affiliation":[{"name":"Center for Vaccine Development,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lei","family":"Zhang","sequence":"additional","affiliation":[{"name":"Center for Vaccine Development,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kari Ann","family":"Shirey","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Janette","family":"Harro","sequence":"additional","affiliation":[{"name":"Graduate Program in Molecular Medicine,"},{"name":"Marlene and Stewart Greenebaum Cancer Center,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeffrey D.","family":"Hasday","sequence":"additional","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine, Department of Medicine,"},{"name":"Department of Pathology, and"},{"name":"Mucosal Biology Research Center, University of Maryland School of Medicine, Baltimore, MD 21201;"},{"name":"Medicine and Research Services, Baltimore Veterans Affairs Medical Center, Baltimore, MD 21201; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Saroj K.","family":"Mohapatra","sequence":"additional","affiliation":[{"name":"Virginia Bioinformatics Institute, Blacksburg, VA 24061"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Oswald R.","family":"Crasta","sequence":"additional","affiliation":[{"name":"Virginia Bioinformatics Institute, Blacksburg, VA 24061"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stefanie N.","family":"Vogel","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology,"},{"name":"Mucosal Biology Research Center, University of Maryland School of Medicine, Baltimore, MD 21201;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alan S.","family":"Cross","sequence":"additional","affiliation":[{"name":"Marlene and Stewart Greenebaum Cancer Center,"},{"name":"Center for Vaccine Development,"},{"name":"Mucosal Biology Research Center, University of Maryland School of Medicine, Baltimore, MD 21201;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bret A.","family":"Hassel","sequence":"additional","affiliation":[{"name":"Graduate Program in Molecular Medicine,"},{"name":"Marlene and Stewart Greenebaum Cancer Center,"},{"name":"Department of Microbiology and Immunology,"},{"name":"Medicine and Research Services, Baltimore Veterans Affairs Medical Center, Baltimore, MD 21201; and"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[2008,12,30]]},"reference":[{"key":"e_1_3_3_1_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.immuni.2006.08.007"},{"key":"e_1_3_3_2_2","first-page":"675","article-title":"The yin and yang of type I interferon activity in bacterial infection","volume":"5","author":"Decker T","year":"2005","unstructured":"T Decker, M Muller, S Stockinger, The yin and yang of type I interferon activity in bacterial infection. 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