{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T22:50:54Z","timestamp":1791154254710,"version":"4.1.0"},"reference-count":31,"publisher":"American Society for Microbiology","issue":"9","license":[{"start":{"date-parts":[[2013,9,1]],"date-time":"2013-09-01T00:00:00Z","timestamp":1377993600000},"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":[[2013,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Francisella tularensis<\/jats:named-content>\n                    , the causative agent of tularemia, is most deadly in the pneumonic form; therefore, mucosal immunity is an important first line of defense against this pathogen. We have now evaluated the lethality of primary\n                    <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">F. tularensis<\/jats:named-content>\n                    live vaccine strain (LVS) pulmonary infection in mice that are defective in IgA (IgA\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice), the predominant mucosal Ig isotype. The results showed that IgA\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice were more susceptible than IgA\n                    <jats:sup>+\/+<\/jats:sup>\n                    mice to intranasal\n                    <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">F. tularensis<\/jats:named-content>\n                    LVS infection, despite developing higher levels of LVS-specific total, IgG, and IgM antibodies in the bronchoalveolar lavage specimens following infection. In addition, the absence of IgA resulted in a significant increase in bacterial loads and reduced survival. Interestingly, IgA\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice had lower pulmonary gamma interferon (IFN-\u03b3) levels and decreased numbers of IFN-\u03b3-secreting CD4\n                    <jats:sup>+<\/jats:sup>\n                    and CD8\n                    <jats:sup>+<\/jats:sup>\n                    T cells in the lung on day 9 postinfection compared to IgA\n                    <jats:sup>+\/+<\/jats:sup>\n                    mice. Furthermore, IgA\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice displayed reduced interleukin 12 (IL-12) levels at early time points, and supplementing IgA\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice with IL-12 prior to LVS challenge induced IFN-\u03b3 production by NK cells and rescued them from mortality. Thus, IgA\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice are highly susceptible to primary pulmonary LVS infections not only because of IgA deficiency but also because of reduced IFN-\u03b3 responses.\n                  <\/jats:p>","DOI":"10.1128\/iai.00408-13","type":"journal-article","created":{"date-parts":[[2013,7,8]],"date-time":"2013-07-08T20:37:28Z","timestamp":1373315848000},"page":"3434-3441","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":21,"title":["Increased Susceptibility of IgA-Deficient Mice to Pulmonary Francisella tularensis Live Vaccine Strain Infection"],"prefix":"10.1128","volume":"81","author":[{"given":"Yoichi","family":"Furuya","sequence":"first","affiliation":[{"name":"Center for Immunology and Microbial Disease, Albany Medical College, Albany, New York, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Girish S.","family":"Kirimanjeswara","sequence":"additional","affiliation":[{"name":"Center for Immunology and Microbial Disease, Albany Medical College, Albany, New York, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sean","family":"Roberts","sequence":"additional","affiliation":[{"name":"Center for Immunology and Microbial Disease, Albany Medical College, Albany, New York, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dennis W.","family":"Metzger","sequence":"additional","affiliation":[{"name":"Center for Immunology and Microbial Disease, Albany Medical College, Albany, New York, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1038\/nrmicro1045"},{"key":"e_1_3_2_3_2","first-page":"61083","article-title":"Possession, use, and transfer of select agents and toxins; biennial review","volume":"77","author":"Federal Register","year":"2012","unstructured":"Federal Register. 2012. Possession, use, and transfer of select agents and toxins; biennial review. Final rule. Fed. Regist. 77:61083\u201361115.","journal-title":"Final rule. Fed. Regist."},{"key":"e_1_3_2_4_2","first-page":"13","article-title":"Overview of the mucosal immune system","volume":"146","author":"Brandtzaeg P","year":"1989","unstructured":"BrandtzaegP. 1989. Overview of the mucosal immune system. Curr. Top. Microbiol. Immunol. 146:13\u201325.","journal-title":"Curr. Top. Microbiol. 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A distinct role for B1b lymphocytes in T cell-independent immunity. Curr. Top. Microbiol. Immunol. 319:105\u2013130.","journal-title":"Curr. Top. Microbiol. Immunol."},{"key":"e_1_3_2_26_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.1202697"},{"key":"e_1_3_2_27_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.0019-2805.2001.01368.x"},{"key":"e_1_3_2_28_2","doi-asserted-by":"crossref","first-page":"2521","DOI":"10.4049\/jimmunol.162.5.2521","article-title":"Targeted deletion of the IgA constant region in mice leads to IgA deficiency with alterations in expression of other Ig isotypes","volume":"162","author":"Harriman GR","year":"1999","unstructured":"HarrimanGRBogueMRogersPFinegoldMPachecoSBradleyAZhangYMbawuikeIN. 1999. Targeted deletion of the IgA constant region in mice leads to IgA deficiency with alterations in expression of other Ig isotypes. J. Immunol. 162:2521\u20132529.","journal-title":"J. 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