{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T19:14:27Z","timestamp":1790190867439,"version":"4.1.0"},"reference-count":82,"publisher":"eLife Sciences Publications, Ltd","license":[{"start":{"date-parts":[[2021,8,23]],"date-time":"2021-08-23T00:00:00Z","timestamp":1629676800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2021,8,23]],"date-time":"2021-08-23T00:00:00Z","timestamp":1629676800000},"content-version":"am","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2021,8,23]],"date-time":"2021-08-23T00:00:00Z","timestamp":1629676800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000060","name":"National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["R01AI109044"],"award-info":[{"award-number":["R01AI109044"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000060","name":"National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["R21AI138550"],"award-info":[{"award-number":["R21AI138550"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000060","name":"National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["R01AI124493"],"award-info":[{"award-number":["R01AI124493"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["elifesciences.org"],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2021,7,31]]},"abstract":"<jats:p>\n                    Arthropod-borne rickettsial pathogens cause mild and severe human disease worldwide. The tick-borne pathogen\n                    <jats:italic>Rickettsia parkeri<\/jats:italic>\n                    elicits skin lesions (eschars) and disseminated disease in humans; however, inbred mice are generally resistant to infection. We report that intradermal infection of mice lacking both interferon receptors (\n                    <jats:italic>\n                      Ifnar1\n                      <jats:sup>-\/-<\/jats:sup>\n                      ;Ifngr1\n                      <jats:sup>-\/-<\/jats:sup>\n                    <\/jats:italic>\n                    ) with as few as 10\n                    <jats:italic>R<\/jats:italic>\n                    .\n                    <jats:italic>parkeri<\/jats:italic>\n                    elicits eschar formation and disseminated, lethal disease. Similar to human infection, eschars exhibited necrosis and inflammation, with bacteria primarily found in leukocytes. Using this model, we find that the actin-based motility factor Sca2 is required for dissemination from the skin to internal organs, and the outer membrane protein OmpB contributes to eschar formation. Immunizing\n                    <jats:italic>\n                      Ifnar1\n                      <jats:sup>-\/-<\/jats:sup>\n                      ;Ifngr1\n                      <jats:sup>-\/-<\/jats:sup>\n                    <\/jats:italic>\n                    mice with\n                    <jats:italic>sca2<\/jats:italic>\n                    and\n                    <jats:italic>ompB<\/jats:italic>\n                    mutant\n                    <jats:italic>R. parkeri<\/jats:italic>\n                    protects against rechallenge, revealing live-attenuated vaccine candidates. Thus,\n                    <jats:italic>\n                      Ifnar1\n                      <jats:sup>-\/-<\/jats:sup>\n                      ;Ifngr1\n                      <jats:sup>-\/-<\/jats:sup>\n                    <\/jats:italic>\n                    mice are a tractable model to investigate rickettsiosis, virulence factors, and immunity. Our results further suggest that discrepancies between mouse and human susceptibility may be due to differences in interferon signaling.\n                  <\/jats:p>","DOI":"10.7554\/elife.67029","type":"journal-article","created":{"date-parts":[[2021,8,23]],"date-time":"2021-08-23T06:00:43Z","timestamp":1629698443000},"update-policy":"https:\/\/doi.org\/10.7554\/elife.67029","source":"Crossref","is-referenced-by-count":32,"title":["Interferon receptor-deficient mice are susceptible to eschar-associated rickettsiosis"],"prefix":"10.7554","volume":"10","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1385-8757","authenticated-orcid":true,"given":"Thomas P","family":"Burke","sequence":"first","affiliation":[{"name":"Molecular and Cell Biology, University of California, Berkeley","place":["Berkeley, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3092-8216","authenticated-orcid":true,"given":"Patrik","family":"Engstr\u00f6m","sequence":"additional","affiliation":[{"name":"Molecular and Cell Biology, University of California, Berkeley","place":["Berkeley, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cuong J","family":"Tran","sequence":"additional","affiliation":[{"name":"Molecular and Cell Biology, University of California, Berkeley","place":["Berkeley, United States"]},{"name":"Division of Infectious Disease and Vaccinology, School of Public Health, University of California, Berkeley","place":["Berkeley, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ingeborg M","family":"Langohr","sequence":"additional","affiliation":[{"name":"Department of Pathobiological Sciences, Louisiana State University","place":["Baton Rouge, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9821-6683","authenticated-orcid":true,"given":"Dustin R","family":"Glasner","sequence":"additional","affiliation":[{"name":"Division of Infectious Disease and Vaccinology, School of Public Health, University of California, Berkeley","place":["Berkeley, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4364-5031","authenticated-orcid":true,"given":"Diego A","family":"Espinosa","sequence":"additional","affiliation":[{"name":"Division of Infectious Disease and Vaccinology, School of Public Health, University of California, Berkeley","place":["Berkeley, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7238-4037","authenticated-orcid":true,"given":"Eva","family":"Harris","sequence":"additional","affiliation":[{"name":"Division of Infectious Disease and Vaccinology, School of Public Health, University of California, Berkeley","place":["Berkeley, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2537-6349","authenticated-orcid":true,"given":"Matthew D","family":"Welch","sequence":"additional","affiliation":[{"name":"Molecular and Cell Biology, University of California, Berkeley","place":["Berkeley, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"4374","published-online":{"date-parts":[[2021,8,23]]},"reference":[{"key":"bib1","doi-asserted-by":"publisher","DOI":"10.1128\/JCM.01728-17","type":"journal-article","article-title":"A concise review of the epidemiology and diagnostics of rickettsioses: Rickettsia and Orientia SPP","volume":"56","author":"Abdad","year":"2018","journal-title":"Journal of Clinical Microbiology"},{"key":"bib2","doi-asserted-by":"publisher","first-page":"132","DOI":"10.1128\/iai.28.1.132-136.1980","type":"journal-article","article-title":"Host defenses in experimental rickettsialpox: Genetics of natural resistance to infection","volume":"28","author":"Anderson","year":"1980","journal-title":"Infect. 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