{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,19]],"date-time":"2026-10-19T19:35:25Z","timestamp":1792438525693,"version":"4.5.0"},"reference-count":41,"publisher":"American Society for Microbiology","issue":"7","license":[{"start":{"date-parts":[[2007,7,1]],"date-time":"2007-07-01T00:00:00Z","timestamp":1183248000000},"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":["Infect Immun"],"published-print":{"date-parts":[[2007,7]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    <jats:italic>Coxiella burnetii<\/jats:italic>\n                    , the etiological agent of Q fever, has two phase variants. Phase I has a complete lipopolysaccharide (LPS), is highly virulent, and causes Q fever in humans and pathology in experimental animals. Phase II lacks an LPS O side chain, is avirulent, and does not grow well in immunocompetent animals. To understand the pathogenicity of Q fever, we investigated the roles of immune components in animals infected with Nine Mile phase I (NM I) or Nine Mile phase II (NM II) bacteria. Immunodeficient mice, including SCID mice (deficient in T and B cells), SCIDbg mice (deficient in T, B, and NK cells), nude mice (deficient in T cells), muMT mice (deficient in B cells), bg mice (deficient in NK cells), mice deficient in tumor necrosis factor alpha (TNF-\u03b1\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice), and mice deficient in gamma interferon (IFN-\u03b3\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice), were compared for their responses to infection. SCID, SCIDbg, nude, and IFN-\u03b3\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice showed high susceptibility to NM I, and TNF-\u03b1\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice showed modest susceptibility. Disease caused by NM I in SCID, SCIDbg, and nude mice progressed slowly, while disease in IFN-\u03b3\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    and TNF-\u03b1\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice advanced rapidly. B- and NK-cell deficiencies did not enhance clinical disease development or alter bacterial clearance but did increase the severity of histopathological changes, particularly in the absence of B cells. Mice infected with NM II showed no apparent clinical disease, but T-cell-deficient mice had histopathological changes. These results suggest that T cells are critical for clearance of\n                    <jats:italic>C. burnetii<\/jats:italic>\n                    , either NM I or NM II, that IFN-\u03b3 and TNF-\u03b1 are essential for the early control of infection, and that B cells are important for the prevention of tissue damage.\n                  <\/jats:p>","DOI":"10.1128\/iai.01767-06","type":"journal-article","created":{"date-parts":[[2007,4,16]],"date-time":"2007-04-16T20:35:40Z","timestamp":1176755740000},"page":"3245-3255","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":151,"title":["T Cells Are Essential for Bacterial Clearance, and Gamma Interferon, Tumor Necrosis Factor Alpha, and B Cells Are Crucial for Disease Development in\n                    <i>Coxiella burnetii<\/i>\n                    Infection in Mice"],"prefix":"10.1128","volume":"75","author":[{"given":"Masako","family":"Andoh","sequence":"first","affiliation":[{"name":"Department of Microbial and Molecular Pathogenesis, Texas A&amp;M University Health Science Center"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guoquan","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Microbial and Molecular Pathogenesis, Texas A&amp;M University Health Science Center"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kasi E.","family":"Russell-Lodrigue","sequence":"additional","affiliation":[{"name":"Department of Microbial and Molecular Pathogenesis, Texas A&amp;M University Health Science Center"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Heather R.","family":"Shive","sequence":"additional","affiliation":[{"name":"Pathobiology Department, College of Veterinary Medicine, Texas A&amp;M University, College Station, Texas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brad R.","family":"Weeks","sequence":"additional","affiliation":[{"name":"Pathobiology Department, College of Veterinary Medicine, Texas A&amp;M University, College Station, Texas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James E.","family":"Samuel","sequence":"additional","affiliation":[{"name":"Department of Microbial and Molecular Pathogenesis, Texas A&amp;M University Health Science Center"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1128\/jb.160.3.994-1002.1984"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.71.8.4717-4723.2003"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1093\/infdis\/170.1.223"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1128\/mr.47.2.127-149.1983"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/0966-842X(94)90542-8"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.72.11.6666-6675.2004"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1128\/JCM.41.5.1869-1874.2003"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.170.8.4217"},{"key":"e_1_3_2_10_2","first-page":"357","volume":"51","year":"2001","unstructured":"Criley, J. 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